Subjects -> BIOLOGY (Total: 3483 journals)
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    - BIOENGINEERING (143 journals)
    - BIOLOGY (1667 journals)
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    - BIOTECHNOLOGY (271 journals)
    - BOTANY (252 journals)
    - CYTOLOGY AND HISTOLOGY (32 journals)
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BIOLOGY (1667 journals)                  1 2 3 4 5 6 7 8 | Last

Showing 1 - 200 of 1720 Journals sorted alphabetically
AAPS Journal     Hybrid Journal   (Followers: 31)
Achievements in the Life Sciences     Open Access   (Followers: 8)
ACS Pharmacology & Translational Science     Hybrid Journal   (Followers: 2)
ACS Synthetic Biology     Hybrid Journal   (Followers: 31)
Acta Biologica Colombiana     Open Access   (Followers: 7)
Acta Biologica Hungarica     Full-text available via subscription   (Followers: 5)
Acta Biologica Sibirica     Open Access   (Followers: 2)
Acta Biologica Turcica     Open Access   (Followers: 1)
Acta Biologica Venezuelica     Open Access  
Acta Biomaterialia     Hybrid Journal   (Followers: 30)
Acta Biotheoretica     Hybrid Journal   (Followers: 3)
Acta Chiropterologica     Full-text available via subscription   (Followers: 6)
acta ethologica     Hybrid Journal   (Followers: 4)
Acta Fytotechnica et Zootechnica     Open Access   (Followers: 1)
Acta Limnologica Brasiliensia     Open Access   (Followers: 4)
Acta Médica Costarricense     Open Access   (Followers: 2)
Acta Musei Silesiae, Scientiae Naturales     Open Access   (Followers: 3)
Acta Neurobiologiae Experimentalis     Open Access  
Acta Parasitologica     Hybrid Journal   (Followers: 12)
Acta Scientiae Biological Research     Open Access   (Followers: 1)
Acta Scientiarum. Biological Sciences     Open Access   (Followers: 2)
Acta Scientifica Naturalis     Open Access   (Followers: 3)
Acta Universitatis Agriculturae et Silviculturae Mendelianae Brunensis     Open Access   (Followers: 1)
Actualidades Biológicas     Open Access   (Followers: 1)
Advanced Biosystems     Hybrid Journal  
Advanced Health Care Technologies     Open Access   (Followers: 10)
Advanced Journal of Graduate Research     Open Access   (Followers: 1)
Advanced Nonlinear Studies     Hybrid Journal  
Advanced Quantum Technologies     Hybrid Journal  
Advanced Studies in Biology     Open Access   (Followers: 1)
Advances in Antiviral Drug Design     Full-text available via subscription   (Followers: 2)
Advances in Bioinformatics     Open Access   (Followers: 20)
Advances in Biological Regulation     Hybrid Journal   (Followers: 4)
Advances in Biology     Open Access   (Followers: 12)
Advances in Biosensors and Bioelectronics     Open Access   (Followers: 8)
Advances in Cell Biology/ Medical Journal of Cell Biology     Open Access   (Followers: 30)
Advances in Cellular and Molecular Biology of Membranes and Organelles     Full-text available via subscription   (Followers: 14)
Advances in Developmental Biology     Full-text available via subscription   (Followers: 14)
Advances in DNA Sequence-Specific Agents     Full-text available via subscription   (Followers: 7)
Advances in Ecological Research     Full-text available via subscription   (Followers: 44)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 19)
Advances in Enzyme Research     Open Access   (Followers: 12)
Advances in Experimental Biology     Full-text available via subscription   (Followers: 9)
Advances in Genome Biology     Full-text available via subscription   (Followers: 11)
Advances in High Energy Physics     Open Access   (Followers: 23)
Advances in Human Biology     Open Access   (Followers: 5)
Advances in Life Science and Technology     Open Access   (Followers: 20)
Advances in Life Sciences     Open Access   (Followers: 7)
Advances in Marine Biology     Full-text available via subscription   (Followers: 21)
Advances in Molecular and Cell Biology     Full-text available via subscription   (Followers: 26)
Advances in Organ Biology     Full-text available via subscription   (Followers: 2)
Advances in Planar Lipid Bilayers and Liposomes     Full-text available via subscription   (Followers: 3)
Advances in Space Biology and Medicine     Full-text available via subscription   (Followers: 7)
Advances in Structural Biology     Full-text available via subscription   (Followers: 6)
Advances in Tropical Biodiversity and Environmental Sciences     Open Access   (Followers: 3)
Advances in Virus Research     Full-text available via subscription   (Followers: 6)
Adversity and Resilience Science : Journal of Research and Practice     Hybrid Journal   (Followers: 2)
African Journal of Range & Forage Science     Hybrid Journal   (Followers: 12)
AFRREV STECH : An International Journal of Science and Technology     Open Access   (Followers: 3)
Ageing Research Reviews     Hybrid Journal   (Followers: 12)
Aging Cell     Open Access   (Followers: 26)
Agrokémia és Talajtan     Full-text available via subscription   (Followers: 2)
Agrokreatif Jurnal Ilmiah Pengabdian kepada Masyarakat     Open Access  
AJP Cell Physiology     Hybrid Journal   (Followers: 18)
AJP Endocrinology and Metabolism     Hybrid Journal   (Followers: 25)
AJP Lung Cellular and Molecular Physiology     Hybrid Journal   (Followers: 3)
Al-Kauniyah : Jurnal Biologi     Open Access  
Alasbimn Journal     Open Access   (Followers: 2)
Alces : A Journal Devoted to the Biology and Management of Moose     Open Access  
AMB Express     Open Access   (Followers: 1)
Ambix     Hybrid Journal   (Followers: 3)
American Biology Teacher     Full-text available via subscription   (Followers: 14)
American Fern Journal     Full-text available via subscription   (Followers: 1)
American Journal of Agricultural and Biological Sciences     Open Access   (Followers: 9)
American Journal of Bioethics     Hybrid Journal   (Followers: 16)
American Journal of Human Biology     Hybrid Journal   (Followers: 18)
American Journal of Medical and Biological Research     Open Access   (Followers: 10)
American Journal of Plant Sciences     Open Access   (Followers: 21)
American Journal of Primatology     Hybrid Journal   (Followers: 16)
American Malacological Bulletin     Full-text available via subscription   (Followers: 3)
American Naturalist     Full-text available via subscription   (Followers: 81)
Amphibia-Reptilia     Hybrid Journal   (Followers: 6)
Anadol University Journal of Science and Technology B : Theoritical Sciences     Open Access  
Anadolu University Journal of Science and Technology : C Life Sciences and Biotechnology     Open Access   (Followers: 2)
Anaerobe     Hybrid Journal   (Followers: 4)
Anales de Biología     Open Access   (Followers: 3)
Analytical Methods     Full-text available via subscription   (Followers: 13)
Anatomical Science International     Hybrid Journal   (Followers: 3)
Animal Cells and Systems     Hybrid Journal   (Followers: 5)
Animal Models and Experimental Medicine     Open Access  
Annales de Limnologie - International Journal of Limnology     Hybrid Journal   (Followers: 1)
Annales françaises d'Oto-rhino-laryngologie et de Pathologie Cervico-faciale     Full-text available via subscription   (Followers: 3)
Annales Henri Poincaré     Hybrid Journal   (Followers: 3)
Annales Universitatis Mariae Curie-Sklodowska, sectio C – Biologia     Open Access   (Followers: 1)
Annals of Applied Biology     Hybrid Journal   (Followers: 8)
Annals of Biomedical Engineering     Hybrid Journal   (Followers: 19)
Annals of Human Biology     Hybrid Journal   (Followers: 6)
Annals of Science and Technology     Open Access  
Annual Research & Review in Biology     Open Access   (Followers: 2)
Annual Review of Biomedical Engineering     Full-text available via subscription   (Followers: 15)
Annual Review of Biophysics     Full-text available via subscription   (Followers: 25)
Annual Review of Cancer Biology     Full-text available via subscription   (Followers: 4)
Annual Review of Cell and Developmental Biology     Full-text available via subscription   (Followers: 42)
Annual Review of Food Science and Technology     Full-text available via subscription   (Followers: 15)
Annual Review of Genomics and Human Genetics     Full-text available via subscription   (Followers: 27)
Annual Review of Phytopathology     Full-text available via subscription   (Followers: 13)
Anthropological Review     Open Access   (Followers: 24)
Antibiotics     Open Access   (Followers: 9)
Antioxidants     Open Access   (Followers: 5)
Antioxidants & Redox Signaling     Hybrid Journal   (Followers: 9)
Antonie van Leeuwenhoek     Hybrid Journal   (Followers: 5)
Anzeiger für Schädlingskunde     Hybrid Journal   (Followers: 1)
Apidologie     Hybrid Journal   (Followers: 5)
Apmis     Hybrid Journal   (Followers: 2)
APOPTOSIS     Hybrid Journal   (Followers: 9)
Applied Biology     Open Access   (Followers: 2)
Applied Bionics and Biomechanics     Open Access   (Followers: 7)
Applied Vegetation Science     Full-text available via subscription   (Followers: 10)
Aquaculture Environment Interactions     Open Access   (Followers: 4)
Aquaculture International     Hybrid Journal   (Followers: 26)
Aquaculture Reports     Open Access   (Followers: 3)
Aquaculture, Aquarium, Conservation & Legislation - International Journal of the Bioflux Society     Open Access   (Followers: 7)
Aquatic Biology     Open Access   (Followers: 8)
Aquatic Ecology     Hybrid Journal   (Followers: 38)
Aquatic Ecosystem Health & Management     Hybrid Journal   (Followers: 16)
Aquatic Science and Technology     Open Access   (Followers: 4)
Aquatic Toxicology     Hybrid Journal   (Followers: 24)
Arabian Journal of Scientific Research / المجلة العربية للبحث العلمي     Open Access   (Followers: 1)
Archaea     Open Access   (Followers: 4)
Archiv für Molluskenkunde: International Journal of Malacology     Full-text available via subscription   (Followers: 3)
Archives of Biological Sciences     Open Access  
Archives of Microbiology     Hybrid Journal   (Followers: 10)
Archives of Natural History     Hybrid Journal   (Followers: 8)
Archives of Oral Biology     Hybrid Journal   (Followers: 3)
Archives of Virology     Hybrid Journal   (Followers: 5)
Archivum Immunologiae et Therapiae Experimentalis     Hybrid Journal   (Followers: 2)
Arctic     Open Access   (Followers: 4)
Arid Ecosystems     Hybrid Journal   (Followers: 3)
Arquivos do Instituto Biológico     Open Access   (Followers: 1)
Arquivos do Museu Dinâmico Interdisciplinar     Open Access  
Arthropod Structure & Development     Hybrid Journal   (Followers: 2)
Arthropods     Open Access   (Followers: 1)
Artificial DNA: PNA & XNA     Hybrid Journal   (Followers: 3)
Asian Bioethics Review     Full-text available via subscription   (Followers: 4)
Asian Journal of Biodiversity     Open Access   (Followers: 5)
Asian Journal of Biological Sciences     Open Access   (Followers: 3)
Asian Journal of Biology     Open Access   (Followers: 2)
Asian Journal of Biotechnology and Bioresource Technology     Open Access   (Followers: 2)
Asian Journal of Cell Biology     Open Access   (Followers: 6)
Asian Journal of Developmental Biology     Open Access   (Followers: 3)
Asian Journal of Medical and Biological Research     Open Access   (Followers: 5)
Asian Journal of Nematology     Open Access   (Followers: 4)
Asian Journal of Poultry Science     Open Access   (Followers: 5)
Atti della Accademia Peloritana dei Pericolanti - Classe di Scienze Medico-Biologiche     Open Access  
Australian Life Scientist     Full-text available via subscription   (Followers: 2)
Australian Mammalogy     Hybrid Journal   (Followers: 8)
Autophagy     Hybrid Journal   (Followers: 4)
Avian Biology Research     Full-text available via subscription   (Followers: 6)
Avian Conservation and Ecology     Open Access   (Followers: 15)
Bacterial Empire     Open Access   (Followers: 1)
Bacteriology Journal     Open Access   (Followers: 1)
Bacteriophage     Full-text available via subscription   (Followers: 3)
Bangladesh Journal of Bioethics     Open Access  
Bangladesh Journal of Plant Taxonomy     Open Access  
Bangladesh Journal of Scientific Research     Open Access   (Followers: 1)
Batman Üniversitesi Yaşam Bilimleri Dergisi     Open Access  
Berita Biologi     Open Access   (Followers: 1)
Between the Species     Open Access   (Followers: 1)
Bio Tribune Magazine     Hybrid Journal  
BIO Web of Conferences     Open Access  
BIO-Complexity     Open Access  
Bio-Grafía. Escritos sobre la Biología y su enseñanza     Open Access  
Bio-Lectura     Open Access  
BIO-SITE : Biologi dan Sains Terapan     Open Access   (Followers: 1)
Bioanalytical Reviews     Hybrid Journal   (Followers: 2)
Biocatalysis and Biotransformation     Hybrid Journal   (Followers: 6)
BioCentury Innovations     Full-text available via subscription   (Followers: 2)
Biochemistry and Cell Biology     Hybrid Journal   (Followers: 16)
Biochimie     Hybrid Journal   (Followers: 5)
BioControl     Hybrid Journal   (Followers: 5)
Biocontrol Science and Technology     Hybrid Journal   (Followers: 8)
Biodemography and Social Biology     Hybrid Journal  
BIODIK : Jurnal Ilmiah Pendidikan Biologi     Open Access   (Followers: 1)
BioDiscovery     Open Access   (Followers: 2)
Biodiversidade e Conservação Marinha : Revista CEPSUL     Open Access  
Biodiversitas : Journal of Biological Diversity     Open Access  
Biodiversity Data Journal     Open Access   (Followers: 4)
Biodiversity Informatics     Open Access   (Followers: 1)
Biodiversity Information Science and Standards     Open Access   (Followers: 2)
Biodiversity: Research and Conservation     Open Access   (Followers: 27)
Bioedukasi : Jurnal Pendidikan Biologi FKIP UM Metro     Open Access  
Bioeksperimen : Jurnal Penelitian Biologi     Open Access  
Bioelectrochemistry     Hybrid Journal   (Followers: 1)
Bioelectromagnetics     Hybrid Journal   (Followers: 2)
Bioenergy Research     Hybrid Journal   (Followers: 3)
Bioengineering and Bioscience     Open Access   (Followers: 3)
BioEssays     Hybrid Journal   (Followers: 11)
Bioethica     Open Access   (Followers: 3)
Bioethics     Hybrid Journal   (Followers: 18)
BioéthiqueOnline     Open Access  

        1 2 3 4 5 6 7 8 | Last

Similar Journals
Journal Cover
Biochemistry and Cell Biology
Journal Prestige (SJR): 0.856
Citation Impact (citeScore): 2
Number of Followers: 16  
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
Published by NRC Research Press Homepage  [21 journals]
  • In Memoriam / In Memoriam
    • Authors: James J. Germida, Suzanne Kettley
      Abstract: Biochemistry and Cell Biology, Volume 98, Issue 2, Page iii-iv, April 2020.

      Citation: Biochemistry and Cell Biology
      PubDate: 2020-04-08T11:27:24Z
      DOI: 10.1139/bcb-2020-0048
      Issue No: Vol. 98, No. 2 (2020)
  • YAP confers resistance to vandetanib in medullary thyroid cancer
    • Authors: Huan Wang, Jian Tang, Zhiwei Su
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Medullary thyroid cancer (MTC) is the third most common thyroid cancer. RET (Rearranged in Transformation) gene mutations are considered as one of the major drivers of MTC. Vandetanib suppresses RET activity, and has shown promise in clinical trials. Unfortunately, acquired resistance to vandetanib has been observed in MTC, although the mechanism was largely unknown. We investigated the critical role of YAP (Yes-Associated Protein) on vandetanib resistance in MTC. For this, TT cells (medullary thyroid cancer cells) were treated with vandetanib for 3 months to generate a vandetanib-resistant cell line (TT-R). We investigated the role of YAP on vandetanib-resistance in TT-R cells by performing cell proliferation and colony formation assays, and examined the antitumor effects of YAP inhibitor and vandetanib in a mouse model of xenografted MTC. The TT-R cells displayed 6-fold higher IC50 to vandetanib than the TT cells. Overexpression of YAP resulted in resistance to vandetanib, whereas knockdown of YAP re-sensitized the TT-R cells to vandetanib. The YAP inhibitor synergized with vandetanib on tumor inhibition. Our results suggest that YAP plays an important role in acquired resistance to vandetanib in MTC, providing basis for combating MTC with YAP inhibitor and vandetanib.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-25T06:51:50Z
      DOI: 10.1139/bcb-2019-0354
  • MicroRNA-760-mediated low expression of DUSP1 impedes the protective
           effect of NaHS on myocardial ischemia–reperfusion injury
    • Authors: Lin Ren, Qian Wang, Lixiang Ma, Dongmei Wang
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Myocardial ischemia–reperfusion injury (MIRI) is the leading cause of the poor prognosis for patients undergoing clinical cardiac surgery. Micro-RNAs are involved in MIRI; however, the effect of miR-760 on MIRI and the molecular mechanisms behind it have not yet been described. For our in-vivo experiments, 20 rats were randomly distributed between 2 groups (n = 10): the sham-treatment group and the ischemia–reperfusion (I/R) group. For our in-vitro experiments, H9C2 cells were subjected to hypoxia for 6 h, and then reoxygenated to establish an hypoxia–reoxygenation (H/R) model. High expression levels of of miR-760 were observed in the rats subjected to MIRI and the H9C2 cells subjected to H/R. Further, the levels of lactate dehydrogenase (LDH) and malonaldehyde (MDA) were increased, and the size of the myocardial infarct was notably greater in the rats subjected to MIRI, suggesting that miR-760 worsens the effects of MIRI. The inhibitory effects from NaHS on apoptosis were enhanced, as were the expression levels of cleaved caspase 3 and cleaved PARP in H9C2 cells exposed to H/R, and with low-expression levels of miR-760. TargetScan and dual luciferase reporter assays further confirmed the targeted relationship between dual-specificity protein phosphatase (DUSP1) and miR-760. Additionally, miR-760 overexpression and H/R treatment of H9C2 cells inhibited the expression of DUSP1, which further promoted apoptosis. Furthermore, DUSP1 enhanced the anti-apoptotic effects of NaHS in rats subjected to MIRI. Taken together, these findings suggest that miR-760 inhibits the protective effect of NaHS against MIRI.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-15T06:41:43Z
      DOI: 10.1139/bcb-2019-0310
  • Protective effect of hydralazine on a cellular model of Parkinson’s
           disease: a possible role of hypoxia-inducible factor (HIF)-1α
    • Authors: Mehrnaz Mehrabani, Mohammad Hadi Nematollahi, Mojde Esmaeili Tarzi, Kobra Bahrampour Juybari, Moslem Abolhassani, Ali Mohammad Sharifi, Hamze Paseban, Mohsen Saravani, Solmaz Mirzamohammadi
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Parkinson’s disease (PD) is a neurodegenerative disease accompanied by a low expression level of cerebral hypoxia-inducible factor (HIF-1α). Hence, activating the hypoxia-signaling pathway may be a favorable therapeutic approach for curing PD. This study explored the efficacy of hydralazine, a well-known antihypertensive agent, for restoring the impaired HIF-1 signaling in PD, with the aid of 6-hydroxydopamine (6-OHDA)-exposed SH-SY5Y cells. The cytotoxicity of hydralazine and 6-OHDA on the SH-SY5Y cells were evaluated by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] and apoptosis detection assays. The activities of malondialdehyde, nitric oxide (NO), ferric reducing antioxidant power (FRAP), and superoxide dismutase (SOD) were also measured. Expression levels of HIF-1α and its downstream genes at the protein level were assessed by Western blotting. Hydralazine showed no toxic effects on SH-SY5Y cells, at the concentration of ≤50 μmol/L. Hydralazine decreased the levels of apoptosis, malondialdehyde, and NO, and increased the activities of FRAP and SOD in cells exposed to 6-OHDA. Furthermore, hydralazine up-regulated the protein expression levels of HIF-1α, vascular endothelial growth factor, tyrosine hydroxylase, and dopamine transporter in the cells also exposed to 6-OHDA, by comparison with the cells exposed to 6-OHDA alone. In summary, hydralazine priming could attenuate the deleterious effects of 6-OHDA on SH-SY5Y cells by increasing cellular antioxidant capacity, as well as the protein levels of HIF-1α and its downstream target genes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-14T04:30:12Z
      DOI: 10.1139/bcb-2019-0117
  • Chondroitin polymerizing factor (CHPF) contributes to malignant
           proliferation and migration of hepatocellular carcinoma cells
    • Authors: Qigang Xu, Wei Lin, Chonglin Tao, Xiaming Huang, Junjian Li
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the human digestive system, and has been recognized as a serious threat to public health worldwide. This study explored the role of chondroitin polymerizing factor (CHPF) in the development and metastasis of HCC. Immunohistochemistry analysis was performed to detect CHPF expression in HCC tissues and para-carcinoma tissues. qRT-PCR and Western blot analysis were used to determine the mRNA and protein expression of CHPF. MTT assays, colony formation assays, and flow cytometry were used to evaluate the cell proliferation, colony formation, and cell apoptosis, respectively. Wound-healing and Transwell assays were performed to evaluate cell migration. The results show that CHPF was not only up-regulated in HCC tissues compared with para-carcinoma tissues, but was also related with more advanced stages of HCC. Further studies revealed that CHPF knockdown significantly inhibited cell proliferation and colony formation, and induce cell apoptosis of HCC cells. Moreover, suppressing the expression of CHPF reduced the migration and invasiveness of HCC cells. In conclusion, we demonstrated that CHPF plays important roles in the development and progression of HCC, and high expression levels of HCC may be related with poorer prognosis. The results from this study may provide a potential therapeutic target for HCC treatment.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-08T05:56:10Z
      DOI: 10.1139/bcb-2019-0227
  • Tetramethylpyrazine ameliorates hepatic fibrosis through
           autophagy-mediated inflammation
    • Authors: Zhigao Hu, Huizhao Su, Yonglian Zeng, Chengjie Lin, Zhenya Guo, Fudi Zhong, Keqing Jiang, Guandou Yuan, Songqing He
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Background: Imbalanced immune response and hepatic fibrosis are key factors related to the progression of chronic liver diseases. Tetramethylpyrazine (TMP), a natural alkaloid, has been widely used for treating liver injury. In this study, we explored the effect of TMP on hepatic fibrosis and the related mechanisms regulating autophagy. Methods: A rat model of hepatic fibrosis and a model using an hepatic stellate cell line (HSC-T6) were created using CCl4 and platelet-derived growth factor (PDGF). Staining with haematoxylin and eosin (HE), Masson’s stain, and TUNEL were performed for pathological diagnosis. ELISA, Western blotting, and immunofluorescence analyses were conducted to determine the expression levels of the specific markers for fibrosis, autophagy, inflammation, and signalling pathways. Results: TMP treatment significantly rescued pathological injury and hepatic fibrosis. It also alleviated imbalances in the immune system, accumulation of extracellular matrix, and autophagy signals in hepatic fibrosis. At the same time, we found that application of the autophagy inducer rapamycin enhanced the therapeutic effect of TMP, whereas the autophagy inhibitor 3-methyladenine, PI3K pathway inhibitor LY294002, and AKT pathway agonist SC79 did the opposite. Conclusions: TMP exerts therapeutic effects in hepatic fibrosis mainly through promoting autophagy to ameliorate inflammation by inhibiting the AKT–mTOR signalling pathway, providing a new perspective for the treatment of chronic liver diseases.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-08T01:42:10Z
      DOI: 10.1139/bcb-2019-0059
  • Long noncoding RNA KCNQ1OT1 is correlated with human breast cancer cell
           development through inverse regulation of hsa-miR-107
    • Authors: Yanyan Wu, Qing-Jun Bi, Rui Han, Yajie Zhang
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      In this work, we investigated the expression pattern and regulatory function of long noncoding RNA (lncRNA) KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in breast cancer. We found that KCNQ1OT1 was significantly upregulated in breast cancer cell lines. In lentiviral-transduced BT-549 and HCC1599 cells, KCNQ1OT1 knockdown impaired cancer cell functions, including in vitro proliferation and migration, and in vivo transplant growth. The possible sponging target of KCNQ1OT1, human microRNA-107 (hsa-miR-107), was confirmed to be bound by KCNQ1OT1, and was upregulated in breast cancer cells with KCNQ1OT1 downregulation. Further, hsa-miR-107 knockdown in KCNQ1OT1-downregulated cancer cells reversed its impairing effects on cancer cell proliferation and migration in vitro. Thus, loss of KCNQ1OT1 is associated with functional impairment in breast cancer cells, likely through inverse regulation of its sponging target, hsa-miR-107.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-05-07T05:02:26Z
      DOI: 10.1139/bcb-2019-0271
  • CEMIP regulates the proliferation and migration of vascular smooth muscle
    • Authors: Qiang Xue, Xiaoli Wang, Xiaohui Deng, Yue Huang, Wei Tian
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      In this study we investigated the regulatory role of cell-migration-inducing and hyaluronan-binding protein (CEMIP) in the proliferation and migration of vascular smooth muscle cells (VSMCs). The mRNA and protein levels of CEMIP were upregulated in the plasma samples from patients with atherosclerosis, and in VSMCs stimulated with platelet-derived growth factor-BB (PDGF-BB), compared with plasma from healthy subjects and untreated VSMCs. Silencing CEMIP suppressed PDGF-BB-induced cell migration and proliferation in VSMCs, as determined using a Cell Counting Kit-8 assays, 5-ethynyl-2′-deocyuridine (EDU) assays, flow cytometry, wound healing assays, and Transwell assays. Overexpression of CEMIP promoted the proliferation and migration of VSMCs via activation of the Wnt–β-catenin signaling pathway and the upregulation of its target genes, including matrix metalloproteinase-2, matrix metalloproteinase-7, cyclin D1, and c-myc, whereas CEMIP deficiency showed the opposite effects. The knockdown of CEMIP in ApoE−/− mice by intravenous injection of lentiviral vector expressing si-CEMIP protected against high-fat-diet-induced atherosclerosis, as shown by the reduced aortic lesion areas, aortic sinus lesion areas, and the concentration of blood lipids compared with mice normally expressing CEMIP. These results demonstrated that CEMIP regulates the proliferation and migration of VSMCs in atherosclerosis by activating the WNT–β-catenin signaling pathway, which suggests the therapeutic potential of CEMIP for the management of atherosclerosis.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-03-24T11:32:29Z
      DOI: 10.1139/bcb-2019-0249
  • Apolipoprotein E2 modulates cell cycle function to promote proliferation
           in pancreatic cancer cells via regulation of the c-Myc–p21Waf1
           signalling pathway
    • Authors: Shaoxia Du, Hui Wang, Jun Cai, Runling Ren, Wenwen Zhang, Wei Wei, Xiaohong Shen
      Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Apolipoprotein E2 (ApoE2) is reportedly critical for cell proliferation and survival, and has been identified as a potential tumour-associated marker in many kinds of cancer. However, studies of the function and mechanisms of ApoE2 in pancreatic cancer proliferation and development are rare. In this study, we performed an analysis to determine the modulatory effects of ApoE2–LRP8 (lipoprotein receptor-related protein 8) pathway on cell cycle and cell proliferation, and explored its mechanisms in pancreatic cancer. High expression levels of ApoE2–LRP8/c-Myc were detected in tumour tissues and cell lines by immunohistochemistry and Western blotting. It was also shown that ApoE2–LRP8 induced phosphorylation of ERK1/2 to activate c-Myc and contribute to cell-cycle-related protein expression. ApoE2 conditions induced c-Myc binding to target gene sequences in the p21Waf1 promoter, resulting in decreased transcription. ERK/c-Myc contributes to the promotion of the expression levels of cyclin D1, cdc2, and cyclin B1, and reduces p21Waf1 activity, thereby promoting cell cycle distribution. We demonstrated the function of ApoE2–LRP8 in the activation of the ERK–c-Myc–p21Waf1 signalling cascade and the modulation of G1/S and G2/M transition, indicating ApoE2–LRP8’s important role in the cancer cell proliferation. ApoE2 could serve as a diagnostic marker and chemotherapeutic target in pancreatic cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-03-13T06:08:44Z
      DOI: 10.1139/bcb-2018-0230
  • Retraction: Grape seed proanthocyanidins ameliorates cadmium-induced renal
           injury and oxidative stress in experimental rats through the up-regulation
           of nuclear related factor 2 and antioxidant responsive elements
    • Authors: Bashir Nazima, Vaihundam Manoharan, Selvaraj Miltonprabu
      Pages: 1 - 1
      Abstract: Biochemistry and Cell Biology, e-First Articles.

      Citation: Biochemistry and Cell Biology
      PubDate: 2020-03-09T02:15:08Z
      DOI: 10.1139/bcb-2020-0070
  • Notch1–Nrf2 signaling crosstalk provides myocardial protection by
           reducing ROS formation
    • Authors: Xue-liang Zhou, Xia Wu, Rong-rong Zhu, Hua Xu, Yun-yun Li, Qi-rong Xu, Sheng Liu, Song-qing Lai, Xinping Xu, Li Wan, Qi-cai Wu, Ji-chun Liu
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Both the Notch1 and Keap1–Nrf2 signaling pathways have cardioprotective effects, but the role of Notch1–Nrf2 crosstalk in myocardial ischemia–reperfusion injury is unclear. In this study, we established hypoxia–reoxygenation in neonate rat myocardial cells and employed γ-secretase inhibitor and curcumin to inhibit and activate the Notch1 and Keap1–Nrf2 signaling pathways, respectively. We found that the combined action of the Notch1 and Keap1–Nrf2 signaling pathways significantly increased cardiomyocyte viability, inhibited cardiomyocyte apoptosis, reduced the formation of reactive oxygen species, and increased antioxidant activities. In conclusion, these findings suggest that Notch1–Nrf2 crosstalk exerts myocardial protection by reducing the formation of reactive oxygen species.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-02-18T05:04:29Z
      DOI: 10.1139/bcb-2018-0398
  • Long noncoding RNA MALAT1 enhances the apoptosis of cardiomyocytes through
           autophagy modulation
    • Authors: Hao Hu, Jiawei Wu, Xiaofan Yu, Junling Zhou, Hua Yu, Likun Ma
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Induction of autophagy promotes cardiomyocyte survival and confers a cardioprotective effect on acute myocardial infarction (AMI). Our previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse AMI. Herein, this study further investigated whether the mechanisms by which MALAT1 enhanced cardiomyocyte apoptosis involved the autophagy regulation. To address this, cardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The cell apoptosis was evaluated using TUNEL staining and Western blot analysis of apoptosis-related proteins. The autophagy level was assessed using GFP-LC3 immunofluorescence and Western blot analysis of autophagy-related proteins. The results showed that H/R injury increased MALAT1 expression. Furthermore, MALAT1 overexpression significantly enhanced apoptosis and regulated autophagy of cardiomyocytes, whereas MALAT1 knockdown exerted the opposite effect. Moreover, rapamycin (an autophagy activator) effectively attenuated the MALAT1-mediated enhancement of cardiomyocyte apoptosis. Overall, our findings demonstrated that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis, at least in part, through autophagy modulation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-01-27T08:00:00Z
      DOI: 10.1139/bcb-2019-0062
  • Ankyrin-B p.S646F undergoes increased proteasome degradation and reduces
           cell viability in the H9c2 rat ventricular cardiomyoblast cell line
    • Authors: Lena Chen, Catherine S.W. Choi, Juan C. Sanchez-Arias, Laura T. Arbour, Leigh Anne Swayne
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Ankyrin-B (AnkB) is scaffolding protein that anchors integral membrane proteins to the cardiomyocyte cytoskeleton. We recently identified an AnkB variant, AnkB p.S646F (ANK2 c.1937 C>T) associated with a phenotype ranging from predisposition for cardiac arrhythmia to cardiomyopathy. AnkB p.S646F exhibited reduced expression levels in the H9c2 rat ventricular-derived cardiomyoblast cell line relative to wildtype AnkB. Here, we demonstrate that AnkB is regulated by proteasomal degradation and proteasome inhibition rescues AnkB p.S646F expression levels in H9c2 cells, although this effect is not conserved with differentiation. We also compared the impact of wildtype AnkB and AnkB p.S646F on cell viability and proliferation. AnkB p.S646F expression resulted in decreased cell viability at 30 h after transfection, whereas we observed a greater proportion of cycling, Ki67-positive cells at 48 h after transfection. Notably, the number of GFP-positive cells was low and was consistent between wildtype AnkB and AnkB p.S646F expressing cells, suggesting that AnkB and AnkB p.S646F affected paracrine communication between H9c2 cells differentially. This work reveals that AnkB levels are regulated by the proteasome and that AnkB p.S646F compromises cell viability. Together, these findings provide key new insights into the putative cellular and molecular mechanisms of AnkB-related cardiac disease.
      Citation: Biochemistry and Cell Biology
      PubDate: 2020-01-22T08:00:00Z
      DOI: 10.1139/bcb-2019-0082
  • miR-140-5p targeted FGF9 and inhibited the cell growth of laryngeal
           squamous cell carcinoma
    • Authors: Ying Wang, Qingli Huang, Faping Li
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Increasing evidence has suggested that microRNAs (miRNAs) play critical roles in the initiation and development of cancers. Here, we found that miR-140-5p was significantly downregulated in both laryngeal squamous cell carcinoma (LSCC) tissues and cell lines. Decreased expression of miR-140-5p was significantly associated with the metastasis of LSCC. Overexpression of miR-140-5p inhibited proliferation and induced apoptosis of LSCC cells. Mechanistically, the fibroblast growth factor 9 (FGF9) was identified as the target of miR-140-5p. miR-140-5p bound the 3′-untranslated region (3′-UTR) of FGF9 and suppressed the expression of FGF9 in LSCC cells. Additionally, the level of FGF9 was upregulated in LSCC tissues and negatively correlated with the expression of miR-140-5p. Restoration of FGF9 attenuated the suppressive role of miR-140-5p in regulating the growth of LSCC cells. Collectively, these results indicated that the tumor suppressive function of miR-140-5p in LSCC was partially exercised by modulating the expression of FGF9.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-12-23T08:00:00Z
      DOI: 10.1139/bcb-2018-0351
  • Active vitamin D activates chondrocyte autophagy to reduce osteoarthritis
           via mediating the AMPK–mTOR signaling pathway
    • Authors: Chunyu Kong, Changlei Wang, Yuquan Shi, Lei Yan, Junhua Xu, Wufang Qi
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Osteoarthritis (OA) is a common joint degenerative disease. Vitamin D (VD) is essential for bone health. We hypothesized that active VD could be used as a therapeutic treatment for OA. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been found in patients with OA, and thus the serum level of VD could be diagnostic of OA. To test this, we established a mouse model of OA. The results from staining with hematoxylin–eosin and Safranin O – Fast Green indicated that active VD reduced the symptoms of OA in mice. The results from Western blotting indicated that treatment with VD increased the activity of the p-AMPK–AMPK signaling pathway and decreased the p-mTOR–mTOR pathway; it also increased the ratio of LC3II:LC3I antibodies and the protein expression levels of Beclin-1, but decreased the level of p62. Further, treatment with VD reduced the levels of tumor necrosis factor-α and interleukin-6 both in cartilage tissues and in chondrocytes. Administration of the AMPK inhibitor compound C and autophagy inhibitor 3-methyladenine (3-MA) reversed these changes following VD treatment. In addition, the results from transfection with mRFP-GFP-LC3 indicated that active VD led to autophagosome aggregation in OA chondrocytes. 3-MA inhibited cell autophagy and promoted inflammation in OA. This study provides evidence that active VD activate chondrocyte autophagy to reduce OA inflammation via activating the AMPK–mTOR signaling pathway. Treatment with active VD could be a novel therapeutic option for OA.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-12-09T08:00:00Z
      DOI: 10.1139/bcb-2019-0333
  • Glycerol kinase enhances hepatic lipid metabolism by repressing nuclear
           receptor subfamily 4 group A1 in the nucleus
    • Authors: Lili Miao, Fei Su, Yongsheng Yang, Yue Liu, Lei Wang, Yiqun Zhan, Ronghua Yin, Miao Yu, Changyan Li, Xiaoming Yang, Changhui Ge
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Glycerol kinase (GYK) plays a critical role in hepatic metabolism by converting glycerol to glycerol 3-phosphate in an ATP-dependent reaction. GYK isoform b is the only glycerol kinase present in whole cells, and has a non-enzymatic moonlighting function in the nucleus. GYK isoform b acts as a co-regulator of nuclear receptor subfamily 4 group A1 (NR4A1) and participates in the regulation of hepatic glucose metabolism by protein–protein interaction with NR4A1. Herein, GYK expression was found to upregulate the expression of NR4A1-mediated lipid metabolism-related genes (SREBP1C, FASN, ACACA, and GPAM) in HEK293T and L02 cells, and in mouse in vivo studies. GYK expression increased blood levels of cholesterol, triglyceride, and high-density lipoprotein cholesterol, but not low-density lipoprotein cholesterol levels. It enhanced the transcriptional activity of Nr4a1 target genes by negatively cooperating with NR4A1 and its enzymatic activity or by other undefined moonlighting functions. This enhancement was observed in both normal and diabetic mice. We also found a feed-forward regulation loop between GYK and NR4A1, serving as part of a GYK-NR4A1 regulatory mechanism in hepatic metabolism. Thus, GYK regulates the effect of NR4A1 on hepatic lipid metabolism in normal and diabetic mice, partially through the cooperation of GYK and NR4A1.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-12-07T08:00:00Z
      DOI: 10.1139/bcb-2019-0317
  • Circ_KATNAL1 regulates prostate cancer cell growth and invasiveness
           through the miR-145-3p/WISP1 pathway
    • Authors: Yu Zheng, Chao-jiang Chen, Zhuo-yuan Lin, Jian-xin Li, Jie Liu, Fu-jun Lin, Xing Zhou
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Prostate cancer (PCa) is the second leading cause of death in men, and current studies have shown that circular RNAs (circRNAs) play important roles in its occurrence and development. Detection of circRNAs in PCa cells showed that circ_KATNAL1 is down-regulated, mainly located in the cytoplasm, and contains multiple binding sites of miR-145-3p, which is an anticancer miRNA. RNA immunoprecipitation with anti-AGO2 antibody, RNA pull-down assays with biotin-labeled circ_KATNAL1 probe or an miR-145-3p mimic, and dual luciferase reporter gene assays confirmed that circ_KATNAL1 binds directly to miR-145-3p in cells, and that WISP1, which is highly expressed in many types of tumors, is an important target gene of miR-145-3p. Circ_KATNAL1 and miR-145-3p promote each other’s expression, and down-regulate the expression of the target gene WISP1. Both circ_KATNAL1 and miR-145-3p inhibit cell proliferation, invasiveness, and migration, down-regulate the expression of MMP-2 and MMP-9, promote cell apoptosis and the activation of caspase-3, caspase-8, caspase-9, and PARP, whereas WISP1 has the opposite effect, and the above-mentioned functions of circ_KATNAL1 were achieved through the miR-145-3p/WISP1 pathway. Therefore, circ_KATNAL1 plays an anticancer role in PCa cells through the miR-145-3p/WISP1 pathway, which could be an important target for the diagnosis and treatment of PCa.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-12-04T08:00:00Z
      DOI: 10.1139/bcb-2019-0211
  • Homogeneity and heterogeneity of biological characteristics in mesenchymal
           stem cells from human umbilical cords and exfoliated deciduous teeth
    • Authors: Chao Yang, Yu Chen, Liwu Zhong, Min You, Zhiling Yan, Maowen Luo, Bo Zhang, Benyanzi Yang, Qiang Chen
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Mesenchymal stem cells (MSCs) have proven powerful potential for cell-based therapy both in regenerative medicine and disease treatment. Human umbilical cords and exfoliated deciduous teeth are the main sources of MSCs with no donor injury or ethical issues. The goal of this study was to investigate the differences in the biological characteristics of human umbilical cord mesenchymal stem cells (UCMSCs) and stem cells from human exfoliated deciduous teeth (SHEDs). UCMSCs and SHEDs were identified by flow cytometry. The proliferation, differentiation, migration, chemotaxis, paracrine, immunomodulatory, neurite growth-promoting capabilities, and acetaldehyde dehydrogenase (ALDH) activity were comparatively studied between these two MSCs in vitro. The results showed that both SHEDs and UCMSCs expressed cell surface markers characteristic of MSCs. Furthermore, SHEDs exhibited better capacity for proliferation, migration, promotion of neurite growth, and chondrogenic differentiation. Meanwhile, UCMSCs showed more outstanding adipogenic differentiation and chemotaxy. Additionally, there were no significant differences in osteogenic differentiation, immunomodulatory capacity, and the proportion of ALDHBright compartment. Our findings indicate that although both UCMSCs and SHEDs are mesenchymal stem cells and presented some similar biological characteristics, they also have differences in many aspects, which might be helpful for developing future clinical cellular therapies.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-12-03T08:00:00Z
      DOI: 10.1139/bcb-2019-0253
  • MiR-539 inhibits the malignant behavior of breast cancer cells by
           targeting SP1
    • Authors: Fenglin Cai, Luhong Chen, Yuting Sun, Chunlan He, Deyuan Fu, Jinhai Tang
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The aberrant expression of microRNAs (miRNAs) is involved in the initiation and progression of human cancers. In our study, we found that miR-539 was down-regulated in breast cancer tissues and cell lines. Decreased expression of miR-539 was significantly associated with lymph node metastasis in patients with breast cancer. Overexpression of miR-539 inhibited the proliferation and promoted apoptosis of breast cancer cells. Moreover, highly expressed miR-539 significantly suppressed the epithelial–mesenchymal transition (EMT) and sensitized cells to cisplatin treatment. Mechanistically, miR-539 was found to target the specificity protein 1 (SP1) and down-regulated the expression of SP1 in breast cancer cells. Knockdown of miR-539 consistently increased the expression of SP1. The expression of miR-539 in breast cancer tissues was negatively correlated with the expression of SP1. Restoration of SP1 significantly attenuated the inhibitory effect of miR-539 on the proliferation of breast cancer cells. Taken together, our results indicate that miR-539 has a tumor suppressive role in breast cancer via targeting SP1, suggesting miR-539 as a promising target for the diagnosis of breast cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-11-19T08:00:00Z
      DOI: 10.1139/bcb-2019-0111
  • PLOD2 promotes aerobic glycolysis and cell progression in colorectal
           cancer by upregulating HK2
    • Authors: Wenwu Du, Ning Liu, Yafeng Zhang, Xi Liu, Yuanhong Yang, Wei Chen, Yi He
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The purpose of this study was to characterize the expression of procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2), a membrane-bound homodimeric enzyme that specifically hydroxylates lysine in the telopeptide of procollagens, and assess the clinical significance of PLOD2 in colorectal cancer (CRC). Our results show that PLOD2 is highly expressed in CRC tumor tissues and cell lines, both at the mRNA and protein levels. Next, we found that PLOD2 was positively correlated with tumor grade (P = 0.001), T stage (P = 0.001), N stage (P < 0.001), and an advanced TNM stage (P < 0.001). Knockdown of PLOD2 attenuated CRC cell proliferation, migration, and invasiveness, in vitro. Our analysis of the mechanism behind the effects of PLOD2 suggests that PLOD2 affected glycolysis by regulating the expression of hexokinase 2 (HK2). HK2 reverses the inhibitory effects of PLOD2 knockdown in CRC. Furthermore, the data suggest that PLOD2 regulates the expression of HK2 via the STAT3 signaling pathway. Survival analysis revealed that high expression levels of PLOD2 (HR = 3.800, P < 0.001) and HK2 expression (HR = 10.222, P < 0.001) correlated with the overall survival rate. After analyzing their expression and correlation, PLOD2 positively correlated with HK2 (r = 0.590, P < 0.001). Our findings have revealed that PLOD2 is a novel regulatory factor in glucose metabolism, exerted via controlling HK2 expression in CRC cells, suggesting PLOD2 as a promising therapeutic target for CRC treatment.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-11-19T08:00:00Z
      DOI: 10.1139/bcb-2019-0256
  • Nicotine-upregulated miR-30a arrests cell cycle in G1 phase by directly
           targeting CCNE2 in human periodontal ligament cells
    • Authors: Lizheng Wu, Kuan Yang, Yajie Gui, Xiaojing Wang
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The consumption of nicotine via smoking tobacco has been reported to stimulate the occurrence and progression of periodontitis. Many studies have demonstrated that nicotine prevents the regeneration of periodontal tissues primarily by inhibiting the proliferation of human periodontal ligament (PDL) cells. However, the mechanisms underlying this process are still unclear. Therefore, we investigated whether nicotine-upregulated miR-30a inhibited the proliferation of human PDL cells by downregulating cyclin E2 (CCNE2), in vitro. Quantitative real-time PCR analysis revealed that nicotine upregulated the expression of miR-30a in human PDL cells. In addition, nicotine inhibited the proliferation of human PDL cells by inducing cell cycle arrest. To support this hypothesis, we showed that nicotine downregulated the expression of CCNE2 in human PDL cells, whereas inhibition of miR-30a restored CCNE2 expression that had been downregulated by nicotine. Furthermore, using luciferase reporter assays, we found that miR-30a directly interacts with the CCNE2 3′UTR. In conclusion, these findings indicate that nicotine-upregulated miR-30a inhibits the proliferation of human PDL cells by downregulating the expression of CCNE2.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-11-05T08:00:00Z
      DOI: 10.1139/bcb-2019-0156
  • Protective effect of nitronyl nitroxide against hypoxia-induced damage in
           PC12 cells
    • Authors: Hongbo Luo, Wei Sun, Jin Shao, Huiping Ma, Zhengping Jia, Linlin Jing
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Hypoxia induces cellular oxidative stress that is associated with neurodegenerative diseases. HPN (4′-hydroxyl-2-substituted phenyl nitronyl nitroxide), a stable nitronyl nitroxide, has excellent free radical scavenging properties. The purpose of this study was to investigate the protective effects of HPN on hypoxia-induced damage in PC12 cells. It was shown that HPN significantly attenuated hypoxia-induced loss of cell viability, release of lactate dehydrogenase (LDH), and morphological changes in PC12 cells. Moreover, hypoxic PC12 cells had increased levels of reactive oxygen species (ROS), malondialdehyde (MDA), and expression of HIF-1α and VEGF, but had reduced levels of superoxide dismutase (SOD) and catalase (CAT), and HPN reversed these changes. HPN also inhibited hypoxia-induced cell apoptosis via suppressing the expression of Bax, cytochrome c, and caspase-3, and inducing the expression of Bcl-2. These results indicate that the protective effects of HPN on hypoxia-induced damage in PC12 cells is associated with the suppression of hypoxia-induced oxidative stress and cell apoptosis. HPN could be a promising candidate for the development of a novel neuroprotective agent.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-11-05T08:00:00Z
      DOI: 10.1139/bcb-2019-0269
  • Connecting proteins: shareable tools for reproducible interaction mapping
    • Authors: Anne-Claude Gingras
      Pages: 1 - 5
      Abstract: Biochemistry and Cell Biology, e-First Articles.

      Citation: Biochemistry and Cell Biology
      PubDate: 2019-11-05T08:00:00Z
      DOI: 10.1139/bcb-2019-0285
  • PML isoform expression and DNA break location relative to PML nuclear
           bodies impacts the efficiency of homologous recombination
    • Authors: Kathleen M. Attwood, Jayme Salsman, Dudley Chung, Sabateeshan Mathavarajah, Carter Van Iderstine, Graham Dellaire
      Pages: 1 - 13
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Promyelocytic leukemia nuclear bodies (PML NBs) are nuclear subdomains that respond to genotoxic stress by increasing in number via changes in chromatin structure. However, the role of the PML protein and PML NBs in specific mechanisms of DNA repair has not been fully characterized. Here, we have directly examined the role of PML in homologous recombination (HR) using I-SceI extrachromosomal and chromosome-based homology-directed repair (HDR) assays, and in HDR by CRISPR/Cas9-mediated gene editing. We determined that PML loss can inhibit HR in an extrachromosomal HDR assay but had less of an effect on CRISPR/Cas9-mediated chromosomal HDR. Overexpression of PML also inhibited both CRISPR HDR and I-SceI-induced HDR using a chromosomal reporter, and in an isoform-specific manner. However, the impact of PML overexpression on the chromosomal HDR reporter was dependent on the intranuclear chromosomal positioning of the reporter. Specifically, HDR at the TAP1 gene locus, which is associated with PML NBs, was reduced compared with a locus not associated with a PML NB; yet, HDR could be reduced at the non-PML NB-associated locus by PML overexpression. Thus, both loss and overexpression of PML isoforms can inhibit HDR, and proximity of a chromosomal break to a PML NB can impact HDR efficiency.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-10-31T07:00:00Z
      DOI: 10.1139/bcb-2019-0115
  • Long noncoding RNA HIF1A-AS2 facilitates cell survival and migration by
           sponging miR-33b-5p to modulate SIRT6 expression in osteosarcoma
    • Authors: Hang Lin, Zhenxu Zhao, Yi Hao, Jun He, Jian He
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Long noncoding RNAs (lncRNAs) are emerging as vital regulators in various physiological and pathological processes. It was recently found that lncRNA HIF1A-AS2 could play oncogenic roles in several cancers. However, the function and regulatory mechanism of lncRNA HIF1A-AS2 in osteosarcoma (OS) remain largely unclear. In this study, we demonstrated that HIF1A-AS2 was overexpressed in OS tissues and cells. Downregulation of HIF1A-AS2 significantly affects multiple biological functions in OS cells, including cell proliferation, cell cycle progression, cell apoptosis, cell migration, and cell invasiveness. Mechanistic investigations demonstrated that HIF1A-AS2 can interact with miR-33b-5p and negatively regulate its expression, thereby upregulating the protein expression of miR-33b-5p’s target SIRT6. Additionally, in vivo experiments using a xenograft tumor mouse model revealed that downregulation of HIF1A-AS2 suppresses tumor growth in OS. Taken together, a newly identified regulatory mechanism for the lncRNA HIF1A-AS2–miR-33b-5p–SIRT6 axis was systematically studied in OS, which could be a promising target for the treatment of OS.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-10-18T07:00:00Z
      DOI: 10.1139/bcb-2019-0171
  • MiR-126 targets IL-17A to enhance proliferation and inhibit apoptosis in
           high-glucose-induced human retinal endothelial cells
    • Authors: Xiujuan Chen, Xuequn Yu, Xinxiang Li, Li Li, Fang Li, Ting Guo, Cuihong Guan, Liping Miao, Guoping Cao
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM), which results in vision loss. This study explored the role of miR-126 in high-glucose-induced human retinal endothelial cells (HRECs) and its underlying molecular mechanisms. The results showed that the expression levels of miR-126 and interleukin-17A (IL-17A) in high-glucose-induced HRECs were downregulated and upregulated, respectively. Functionally, overexpression of miR-126 promoted proliferation and suppressed apoptosis in high-glucose-induced HRECs, while IL-17A reversed the effects induced by miR-126. However, overexpression of IL-17A inhibited the proliferation and induced apoptosis, while knockdown of IL-17A accelerated the proliferation and repressed apoptosis. In addition, miR-126 repressed the expression of IL-17A, Bax, and caspase-3, while promoting the expression of survivin and phosphorylation of PI3K and AKT; restoration of IL-17A rescued these effects. Furthermore, IL-17A was identified as a target of miR-126. This indicates that miR-126 enhances proliferation and inhibits apoptosis in high-glucose-induced HRECs by activating the PI3K–AKT pathway, increasing survivin levels, and decreasing Bax and caspase-3 expression by targeting IL-17A, suggesting that miR-126 could be a novel target for preventing DR.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-10-13T07:00:00Z
      DOI: 10.1139/bcb-2019-0174
  • Subcellular fractionation of frozen skeletal muscle samples
    • Authors: Pedro Rafael Firmino Dias, Paulo Guimarães Gandra, René Brenzikofer, Denise Vaz Macedo
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Cell fractionation can be used to determine the localization and trafficking of proteins between cellular compartments such as the cytosol, mitochondria, and nuclei. Subcellular fractionation is usually performed immediately after tissue dissection because freezing may fragment cell membranes and induce organellar cross-contamination. Mitochondria are especially sensitive to freezing/thawing and mechanical homogenization. We proposed a protocol to improve the retention of soluble proteins in the mitochondrial fraction obtained from small amounts of frozen skeletal muscle. Fifty milligrams of the red portion of gastrocnemius muscle from Wistar rats were immediately processed or frozen in liquid nitrogen and stored at −80 °C for further processing. We compared the enrichment of subcellular fractions from frozen/fresh samples obtained with the modified protocol with those obtained by standard fractionation. Western blot analyses of marker proteins for cytosolic (alpha-tubulin), mitochondrial (VDAC1), and nuclear (histone-H3) fractions indicated that all of the procedures resulted in enriched subcellular fractions with minimal organellar cross-contamination. Notably, the activity of the soluble protein citrate synthase was higher in the mitochondrial fractions obtained with the modified protocol from frozen/fresh samples compared with the standard protocol. Therefore, our protocol improved the retention of soluble proteins in the mitochondrial fraction and may be suitable for subcellular fractionation of small amounts of frozen skeletal muscle samples.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-10-12T07:00:00Z
      DOI: 10.1139/bcb-2019-0219
  • MicroRNA-1298-5p inhibits cell proliferation and the invasiveness of
           bladder cancer cells via down-regulation of connexin 43
    • Authors: Gang Li, Longfeng Sun, Zhongyi Mu, Shibo Liu, Hongchen Qu, Qingpeng Xie, Bin Hu
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      MicroRNA (miR)-1298 is widely down-regulated in a variety of malignant tumors, which facilitates cell proliferation, invasiveness, and migration. However, the specific biological function of miR-1298 in bladder cancer (BC) is still unknown. Connexin 43 (Cx43) is often up-regulated in tumors. Identifying miRNAs that target Cx43 in the setting of BC will help to develop Cx43-based therapies for BC. In this study, the results demonstrated that the expression levels of miR-1298 and Cx43 were significantly down-regulated and up-regulated, respectively, in BC tissues. Overexpression of miR-1298 inhibited cell proliferation, migration, and invasiveness in two BC cell lines as determined using MTT assays, cell cycle assays, colony formation assays, Transwell assays, gelatin zymography, and Western blot. In addition, we found that miR-1298 decreased Cx43 expression by directly targeting the 3′-UTR. Further, we observed that the promotion of BC cell proliferation, migration, and invasiveness from Cx43 on could be partially attenuated by overexpressing miR-1298. Moreover, the protein expression of p-ERK was ameliorated after transfection with overexpressed-miR-1298. Knockdown of Cx43 reversed the promotion of cell migration and invasiveness due to decreased expression of miR-1298. All of the data from our study indicate that miR-1298 could be a diagnostic marker of BC and a potential therapeutic agent via inhibiting Cx43.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-10-10T07:00:00Z
      DOI: 10.1139/bcb-2019-0137
  • Extracellular pyruvate kinase M2 facilitates cell migration by
           upregulating claudin-1 expression in colon cancer cells
    • Authors: Hyunju Kim, Seong Ho Kim, Dohyeon Hwang, Jinsu An, Hak Suk Chung, Eun Gyeong Yang, So Yeon Kim
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Extensive studies have been reported the non-canonical functions of pyruvate kinase M2 (PKM2) as a kinase, transcriptional regulator, and even cell-to-cell communicator, emphasizing its importance in various signaling pathways. However, the role of secreted PKM2 in cancer progression and its signaling pathway is yet to be elucidated. In this study, we found that extracellular PKM2 enhanced the migration of low-metastatic, benign colon cancer cells by upregulating claudin-1 expression and internalizing it to the cytoplasm and nucleus. Knock-down of claudin-1 significantly reduced extracellular PKM2-induced cell migration. Inhibition of either protein kinase C (PKC) or epidermal growth factor receptor (EGFR) resulted in a reduction of extracellular PKM2-mediated claudin-1 expression, suggesting EGFR–PKC–claudin-1 as a signaling pathway in the extracellular PKM2-mediated tumorigenesis of colon cancer cells.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-09-23T07:00:00Z
      DOI: 10.1139/bcb-2019-0139
  • MicroRNA-24 alleviates isoflurane-induced neurotoxicity in rat hippocampus
           via attenuation of oxidative stress
    • Authors: Na Li, Linli Yue, Jun Wang, Zhenzhen Wan, Wenhao Bu
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Several miRNAs have been recently suggested as potential therapeutic targets for anesthesia-related diseases. This study was carried out to explore the biological roles of miR-24 in isoflurane-treated rat hippocampal neurons. Isoflurane was used to induce neurotoxicity in a rat model. Gain- and loss-of-function of miR-24 was performed, and the size and Ca2+ permeability of mitochondria, as well as cell proliferation and apoptosis, and levels of oxidative-stress-related factors were measured both in vivo and in vitro. Dual luciferase reporter gene assays were used to identify the target relationship between miR-24 and p27kip1. In this study, isoflurane treatment decreased miR-24 expression, after which, levels of neuron apoptosis and oxidative-stress-related factors were elevated and neuron viability was reduced. Over-expression of miR-24 inhibited oxidative damage and neuronal apoptosis in hippocampal tissues, and suppressed the size and Ca2+ permeability of mitochondria of hippocampal neurons. miR-24 enhanced the viability of rat hippocampal neurons by targeting p27kip1. To conclude, this study demonstrated that miR-24 attenuates isoflurane-induced neurotoxicity in rat hippocampus via its antioxidative properties and inhibiting p27kip1 expression.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-09-18T07:00:00Z
      DOI: 10.1139/bcb-2019-0188
  • MicroRNA profiling of human myeloid angiogenic cells derived from
           peripheral blood mononuclear cells
    • Authors: Qiuwang Zhang, Anthony Cannavicci, Si-Cheng Dai, Chenxi Wang, Michael J.B. Kutryk
      Pages: 1 - 5
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Human myeloid angiogenic cells (MACs), also termed early endothelial progenitor cells, play an important role in neovascularization and vascular repair. MicroRNAs (miRNAs) are a class of naturally occurring, noncoding, short (∼22 nucleotides), single-stranded RNAs that regulate gene expression post-transcriptionally. MiRNAs have been shown to regulate MAC function. A miRNA signature of MACs was described approximately a decade ago, and many new miRNAs have been discovered in recent years. In this study, we aimed to provide an up-to-date miRNA signature for human MACs. MACs were obtained by culture of human peripheral blood mononuclear cells in endothelial medium for 7 days. Using qPCR array analysis we identified 72 highly expressed miRNAs (CT value < 30) in human MACs. RT–qPCR quantification of select miRNAs revealed a strong correlation between the CT values detected by the array analysis and RT–qPCR, suggesting the miRNA signature generated by the qPCR array assay is accurate and reliable. Experimentally validated target genes of the 10 most highly expressed miRNAs were retrieved. Only a few of the targets and their respective miRNAs have been studied for their role in MAC biology. Our study therefore provides a valuable repository of miRNAs for future exploration of miRNA function in MACs.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-09-04T07:00:00Z
      DOI: 10.1139/bcb-2019-0163
  • Genes responsive to rapamycin and serum deprivation are clustered on
           chromosomes and undergo reorganization within local chromatin environments
    • Authors: Zachery R. Belak, Joshua. A. Pickering, Zoe. E. Gillespie, Gerald Audette, Mark Eramian, Jennifer. A. Mitchell, Joanna. M. Bridger, Anthony Kusalik, Christopher H. Eskiw
      Pages: 1 - 13
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      We previously demonstrated that genome reorganization, through chromosome territory repositioning, occurs concurrently with significant changes in gene expression in normal primary human fibroblasts treated with the drug rapamycin, or stimulated into quiescence. Although these events occurred concomitantly, it is unclear how specific changes in gene expression relate to reorganization of the genome at higher resolution. We used computational analyses, genome organization assays, and microscopy, to investigate the relationship between chromosome territory positioning and gene expression. We determined that despite relocation of chromosome territories, there was no substantial bias in the proportion of genes changing expression on any one chromosome, including chromosomes 10 and 18. Computational analyses identified that clusters of serum deprivation and rapamycin-responsive genes along the linear extent of chromosomes. Chromosome conformation capture (3C) analysis demonstrated the strengthening or loss of specific long-range chromatin interactions in response to rapamycin and quiescence induction, including a cluster of genes containing Interleukin-8 and several chemokine genes on chromosome 4. We further observed that the LIF gene, which is highly induced upon rapamycin treatment, strengthened interactions with up- and down-stream intergenic regions. Our findings indicate that the repositioning of chromosome territories in response to cell stimuli, this does not reflect gene expression changes occurring within physically clustered groups of genes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-09-03T07:00:00Z
      DOI: 10.1139/bcb-2019-0096
  • Silencing LINC00511 inhibits cell proliferation, migration, and
           epithelial–mesenchymal transition via the PTEN–AKT–FOXO1 signaling
           pathway in lung cancer
    • Authors: Lianyong Jiang, Xiao Xie, Fangbao Ding, Ju Mei, Rui Bi
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Lung cancer is the most common cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) are longer than 200 nt transcripts and are not translated into proteins. Increasing evidence has shown that lncRNAs are associated with several biological processes in cancer. However, the roles of LINC00511 in lung cancer progression remain unknown. In the present study, we confirmed that LINC00511 knockdown significantly inhibited cell proliferation and migration in A549, SPCA1, and H460 cells. Western blot results showed that silencing LINC00511 inhibited epithelial–mesenchymal transition (EMT), which resulted in decreased expression levels of ZEB2, N-cadherin, and vimentin and increased expression levels of E-cadherin. Additionally, silencing LINC00511 significantly upregulated PTEN mRNA and protein expression, increased FOXO1, and inactivated AKT. Furthermore, we found that PTEN knockdown reversed the inhibition of cell migration and proliferation induced by LINC00511 siRNA, markedly reduced p-FOXO1 expression, and promoted p-AKT expression and EMT in A549 and H460 cells. Therefore, these findings revealed that LINC00511 functions as an oncogene through the PTEN–AKT–FOXO1 signaling pathway in lung cancer, providing a potential target of metastasis in lung cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-08-15T07:00:00Z
      DOI: 10.1139/bcb-2018-0364
  • RP5-1120P11.3 promotes hepatocellular carcinoma development via the
           miR-196b-5p–WIPF2 axis
    • Authors: Hongjun Zhai, Xinwu Zhang, Shuo Chen, Meng Fan, Shuangyu Ma, Xiaoli Sun
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Hepatocellular carcinoma (HCC) remains a huge threat to human health even though the diagnosis and treatment strategies have improved rapidly in the past few decades. Increasing evidence has illustrated the critical role noncoding RNA and their regulatory network play in the pathology of HCC. Here, we identified a novel long noncoding RNA, RP5-1120P11.3, that is ectopically expressed in HCC. Further characterization of RP5-1120P11.3 revealed that it promoted proliferation and invasion of HCC cells while inhibiting apoptosis. Importantly, our data revealed that miR-196b-5p interacted with and was regulated by RP5-1120P11.3 via a sponging mechanism. Inhibition of miR-196b-5p attenuated the phenotypes resulting from RP5-1120P11.3 inhibition. Moreover, our data showed that miR-196b-5p inhibited the expression of WIPF2 in HCC, illustrating a regulatory axis of RP5-1120P11.3–miR-196b-5p–WIPF2 that facilitated the progression of HCC. In addition, our data showed that RP5-1120P11.3 contributed to xenograft generation in vivo by regulating miR-196b-5p and WIPF2. These findings suggested that the RP5-1120P11.3–miR-196b-5p–WIPF2 axis is a potential target for treatment of HCC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-07-12T07:00:00Z
      DOI: 10.1139/bcb-2019-0053
  • Atypical chromatin structure of immune-related genes expressed in chicken
    • Authors: Sanzida Jahan, Tasnim H. Beacon, Wayne Xu, James R. Davie
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The major biological role of red blood cells is to carry oxygen to the tissues in the body. However, another role of the erythroid cell is to participate in the immune response. Mature erythrocytes from chickens express Toll-like receptors and several cytokines in response to stimulation of the immune system. We previously reported the application of a biochemical fractionation protocol to isolate highly enriched transcribed DNA from polychromatic erythrocytes from chickens. In conjunction with next-generation DNA, RNA sequencing, chromatin immunoprecipitation-DNA sequencing, and formaldehyde-assisted isolation of regulatory elements (FAIRE) sequencing, we identified the active chromosomal compartments and determined their structural signatures in relation to expression levels. Here, we present the detailed chromatin characteristics of erythroid genes participating in the innate immune response. Our studies revealed an atypical chromatin structure for several genes coding for Toll-like receptors, interleukins, and interferon regulatory factors. The body of these genes had nucleosome-free regions intermingled with nucleosomes modified with H3K4me3 and H3K27ac, suggesting a dynamic unstable chromatin structure. We further show that human genes involved in cell identity have gene bodies with the same chromatin-instability features as the chicken polychromatic erythrocyte genes participating in the innate immune response.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-07-05T07:00:00Z
      DOI: 10.1139/bcb-2019-0107
  • circ-NOTCH1 acts as a sponge of miR-637 and affects the expression of its
           target gene Apelin to regulate gastric cancer cell growth
    • Authors: Encui Guan, Xiaoguang Xu, Fangxi Xue
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Gastric cancer (GC) is a major cause of cancer-related deaths worldwide, and has a low survival rate, low cure rate, high recurrence rate, and poor prognosis. Recent studies have indicated that circular RNAs (circRNAs) have important functions in the occurrence and progression of GC. Studies on circ-NOTCH1, which was shown to be highly expressed in GC, have indicated that miR-637 binds to circ-NOTCH1 at multiple sites, and a dual-luciferase reporter gene assay further confirmed that miR-637 indeed targeted circ-NOTCH1 and Apelin. Circ-NOTCH1 and Apelin are highly expressed in GC cells and tissues, whereas the expression of miR-637 is reduced. Circ-NOTCH1 and miR-637 do not regulate each other’s expression levels, but circ-NOTCH1significantly upregulates the expression of the miR-637 target gene Apelin, whereas miR-637 inhibites the expression of Apelin. Examination of GC cells showed that circ-NOTCH1 enhances cell proliferation and invasiveness, and reduces cell apoptosis; these effects were reversed by miR-637, which could terminate the above effects of circ-NOTCH1. When co-transfected with the circ-NOTCH1 overexpression plasmid and Apelin siRNAs, there were no obvious changes to the levels of cell proliferation, apoptosis, or invasiveness. Therefore, in GC cells, circ-NOTCH1 inhibits the transcriptional activity of miR-637, thereby upregulating the expression of its target gene Apelin and regulating cell proliferation, apoptosis, and invasiveness. This finding provides more experimental evidence for the function of circRNA in GC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-07-05T07:00:00Z
      DOI: 10.1139/bcb-2019-0079
  • MicroRNA-378-3p/5p suppresses the migration and invasiveness of oral
           squamous carcinoma cells by inhibiting KLK4 expression
    • Authors: Zhi Cui, Shiqun Sun, Qilin Liu, Xuechun Zhou, Siyu Gao, Peixuan Peng, Qianpeng Li
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Distant metastasis frequently occurs in oral squamous cell carcinoma (OSCC) and contributes to the adverse prognosis for patients with OSCC. However, the potential mechanisms behind the metastasis have not yet been clarified. This study investigated the role of miR-378 in the migration and invasiveness of OSCC in vitro and in vivo. According to our results, the migration and invasiveness of OSCC cells were increased in cells overexpressing miR-378, and reduced in cells where miR-378-3p/5p was silenced. In addition, overexpression of miR-378 suppressed the expressions and activities of matrix metalloproteinase 9 (MMP-9) and MMP-2. Epithelial–mesenchymal transition (EMT) was restrained by overexpression of miR-378, as evidenced by an increase in E-cadherin expression and decrease in N-cadherin and uPA expression. However, knockdown of miR-378-3p/5p produced the opposite results. Moreover, kallikrein-related peptidase 4 (KLK4) was confirmed to be a target gene of miR-378. Overexpression of KLK4 reversed the induced decrease in migration and invasiveness of cells overexpressing miR-378 by upregulating the levels of MMP-9, MMP-2, and N-cadherin, and downregulating the level of E-cadhrin. Finally, the number of metastasis nodules in the lung tissues of nude mice was reduced by overexpression of miR-378, whereas the number of metastases increased with knockdown of miR-378. Taken together, our results suggest that the miR-378–KLK4 axis is involved in the mechanisms behind the migration and invasiveness of OSCC cells. Targeting the miR-378–KLK4 axis may be an effective measure for treating OSCC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-07-02T07:00:00Z
      DOI: 10.1139/bcb-2019-0017
  • DNA methylation and regulation of DNA methyltransferases in a
           freeze-tolerant vertebrate
    • Authors: Jing Zhang, Liam J. Hawkins, Kenneth B. Storey
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The wood frog is one of the few freeze-tolerance vertebrates. This is accomplished in part by the accumulation of cryoprotectant glucose, metabolic rate depression, and stress response activation. These may be achieved by mechanisms such as DNA methylation, which is typically associated with transcriptional repression. Hyperglycemia is also associated with modifications to epigenetic profiles, indicating an additional role that the high levels of glucose play in freeze tolerance. We sought to determine whether DNA methylation is affected during freezing exposure, and whether this is due to the wood frog’s response to hyperglycemia. We examined global DNA methylation and DNA methyltransferases (DNMTs) in the liver and muscle of frozen and glucose-loaded wood frogs. The results showed that levels of 5-methylcytosine (5mC) increased in the muscle, suggesting elevated DNA methylation during freezing. DNMT activities also decreased in muscle during thawing, glucose loading, and in vitro glucose experiments. Liver DNMT activities were similar to muscle; however, a varied response to DNMT levels and a decrease in 5mC highlight the metabolic role the liver plays during freezing. Glucose was also shown to decrease DNMT activity levels in the wood frog, in vitro, elucidating a potentially novel regulatory mechanism. Together these results suggest an interplay between freeze tolerance and hyperglycemic regulation of DNA methylation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-05-22T07:00:00Z
      DOI: 10.1139/bcb-2019-0091
  • MicroRNA-211-5p promotes apoptosis and inhibits the migration of
           osteosarcoma cells by targeting proline-rich protein PRR11
    • Authors: Dandan Song, Kun Yang, Wei Wang, Run Tian, Haoyu Wang, Kunzheng Wang
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Osteosarcoma remains fatal in adolescents and young adults, with a 5-year survival rate of less than 20%. However, the details for mechanisms that regulate osteosarcoma metastasis are poorly understood. We analyzed the expression levels of miR-211-5p in clinical samples of osteosarcoma as well as cell lines, and found that the expression of miR-211-5p was reduced in osteosarcoma. Moreover, induction of miR-211-5p in several osteosarcoma cell lines dramatically inhibited their migration and invasiveness. Furthermore, miR-211-5p overexpression led to a significant increase in the apoptosis of osteosarcoma cell. Importantly, our in vivo xenograft experiments showed that miR-211-5p strongly inhibits tumorigenesis. Additionally, functional experiments demonstrated that miR-211-5p suppresses the expression of proline-rich protein 11 (PRR11) by directly binding to the 3′ region of PRR11 mRNA. Moreover, we showed that PRR11 overexpression attenuated the increase of apoptosis and decreased migration and invasiveness when the upstream miR-211-5p was overexpressed. Our data provide new insights into the mechanisms that regulate osteosarcoma metastasis, and novel potential pharmaceutical targets for personalized medicine.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-05-10T07:00:00Z
      DOI: 10.1139/bcb-2018-0380
  • Mitochondrial dysfunction regulates the JAK–STAT pathway via
           LKB1-mediated AMPK activation ER-stress-independent manner
    • Authors: Dong-Yeon Kim, Su-Geun Lim, Kyoungho Suk, Won-Ha Lee
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Mitochondria affect cellular functions alone or in cooperation with other cellular organelles. Recent research has demonstrated the close relationship of mitochondria with the endoplasmic reticulum (ER), both at the physical and the functional level. In an effort to define the combined effect of mitochondrial dysfunction (MD) and ER stress in the proinflammatory activities of macrophages, the human macrophage-like monocytic leukemia cell line THP-1 was treated with mitochondrial electron transport chain (ETC) blockers, and changes in the cellular responses upon stimulation by interferon (IFN)-γ were analyzed. Inducing mitochondrial dysfunction (MD) with ETC blockers resulted in suppression of IFN-induced activation of JAK1 and STAT1/3, as well as the expression of STAT1-regulated genes. In addition, experiments utilizing pharmacological modulators of adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1–AMPK pathway. Treatment with pharmacological inhibitors of ER stress sensors failed to affect these processes, thus indicating that involvement of ER stress is not required. These results indicate that MD, induced by blocking the ETC, affects IFN-induced activation of JAK–STAT and associated inflammatory changes in THP-1 cells through the LKB1–AMPK pathway independently of ER stress.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-05-09T07:00:00Z
      DOI: 10.1139/bcb-2019-0088
  • Sirt6 stabilizes atherosclerosis plaques by promoting macrophage autophagy
           and reducing contact with endothelial cells
    • Authors: Tingting Wang, Chuang Sun, Lang Hu, Erhe Gao, Congye Li, Haichang Wang, Dongdong Sun
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Sirt6 has been reported to play a protective role in macrophage foam cell formation, but whether Sirt6 controls atherosclerosis plaque stability and whether it can reduce the interaction between endothelial cells and macrophages remains unclear. The aim of this study was to investigate the effect of Sirt6 on atherosclerosis plaque stability and the underlying mechanisms. We used Tie2-Cre transgenic mice as a Cre-lox tool to delete Sirt6 floxed sequences in endothelial cells during adulthood to establish Sirt6−/− mice. ApoE−/−:Sirt6−/− and ApoE−/−:Sirt6Tg mice were used in our investigation. After a 16 week high-fat diet, the mice developed markedly atherosclerotic plaques. Sirt6 knockout exacerbated atherosclerotic plaque progression in both size and stability. In vitro, murine macrophage RAW264.7 cells were treated with ox-low density lipoproteins for 24 h to simulate atherosclerosis. Furthermore, Sirt6 overexpression remarkably increased autophagic flux in macrophages and inhibited macrophage apoptosis. Moreover, Sirt6 overexpression inhibited the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and platelet selectin (P-selectin), leading to reduced infiltration of macrophages and foam cells. In conclusion, our study indicates a new mechanism-based strategy to therapeutically stimulate atherosclerosis plaque stability.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-05-07T07:00:00Z
      DOI: 10.1139/bcb-2019-0057
  • Role of syndecan-1 and exogenous heparin in hepatoma sphere formation
    • Authors: Shih-Chiang Lin, Ching-Po Wu, TingTing Tseng, Yaoyun Jhang, Shao-Chen Lee
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Glycosaminoglycan-modified proteoglycans play important roles in many cell activities, including cell differentiation and stem cell development. Tumor sphere formation ability is one of properties in cancer stem cells (CSCs). The correlation between CSC markers and proteoglycan remains to be clarified. Upon hepatoma sphere formation, expression of CSC markers CD13, CD90, CD133, and CD44, as well the syndecan family protein syndecan-1 (SDC1), increased as analyzed by PCR. Further examination by suppression of CD13 expression showed downregulation of SDC1 and CD44 gene expression, whereas suppression of SDC1 gene expression downregulated CD13 and CD44 gene expression. Suppression of SDC1 gene expression also suppressed sphere development, as analyzed by a novel sphereocrit assay to quantify the level of sphere formation. The heparin disaccharide components, but not those of chondroitin disaccharide, changed with hepatoma sphere development, revealing the increased levels of N-sulfation and 2-O-sulfation. These explained the inhibition of hepatoma sphere formation by exogenous heparin. In conclusion, we found that SDC1 affected CSC marker CD13 and CD44 expression. SDC1 proteoglycan and heparin components changed and affected hepatoma sphere development. Application of heparin mimics in reduction of hepatoma stem cells might be possible.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-05-01T07:00:00Z
      DOI: 10.1139/bcb-2018-0246
  • miR-628-5p promotes growth and migration of osteosarcoma by targeting
    • Authors: Ju-Yong Wang, Ju-Qiang Wang, Shi-Bao Lu
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      This study investigated the role of miR-628-5p and interferon-induced protein 44-like (IFI44L) in osteosarcoma (OS) and determined whether miR-628-5p modulated OS growth by regulating IFI44L. Based on the data downloaded from Gene Expression Omnibus (GEO) database, we revealed that the expression of IFI44L was downregulated in OS and low expression of IFI44L was correlated with better prognosis of patients with OS. Biological prediction of its upstream regulatory miRNAs on the miRWalk website found that miR-628-5p is a possible upstream regulatory miRNA of IFI44L. Luciferase activity assay demonstrated that miR-628-5p could bind to the 3′ untranslated region (UTR) of IFI44L, which proved the above prediction. The expression of miR-628-5p is upregulated in OS and high expression of miR-628-5p is correlated with poor prognosis of patients with OS. The results of RT-qPCR showed that the expression of miR-628-5p in MG-63, U2OS, Saos-2, and SW1353 cells was significantly higher than that in the hFOB1.19 cells. Downregulation of miR-628-5p by miR-628-5p inhibitor significantly inhibited the proliferation, migration, and invasion of MG-63 cells. By rescue assay, we found that knockdown of IFI44L rescued the proliferation and motility of miR-628-5p depleted MG-63 cells. Collectively, our present data illustrated that miR-628-5p promoted the growth and motility of OS at least partly by targeting IFI44L. Moreover, miR-628-5p and IFI44L might be proposed as promising biomarkers in OS diagnosis and treatment.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-04-24T07:00:00Z
      DOI: 10.1139/bcb-2019-0001
  • Long noncoding RNA XIST regulates the EGF receptor to promote
           TGF-β1-induced epithelial–mesenchymal transition in pancreatic cancer
    • Authors: Lei Zou, Feng-Rong Chen, Ren-Pin Xia, Hua-Wei Wang, Zhen-Rong Xie, Yu Xu, Jue-Hua Yu, Kun-Hua Wang
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Background: This study focuses on the lncRNA XIST (X inactive-specific transcript), an lncRNA involved in multiple human cancers, and investigates the functional significance of XIST and the molecular mechanisms underlying the epithelial–mesenchymal transition (EMT) in pancreatic cancer (PC). Methods: Clinical specimens from 25 patients as well as 5 human PC cell lines were analyzed for XIST, YAP, and microRNA(miR)-34a by quantitative real-time PCR (qRT-PCR) and immunohistochemistry. To investigate how XIST influences cell proliferation, invasiveness, and apoptosis in PC, we performed the CCK-8 assays, Transwell assays, and flow cytometry. Luciferase reporter assays, qRT-PCR, and Western blot were applied to prove that miR-34a directly binds to XIST. Results: Up-regulation of XIST and Yes associated protein (YAP) and down-regulation of miR-34a were consistently observed in the clinical specimens and PC cell lines. Silencing XIST reduced the expression of YAP and suppressed transforming growth factor (TGF)-β1-induced EMT, while over-expression of XIST increased the expression of YAP and promoted EMT. In addition, inhibition of epidermal growth factor receptor (EGFR) hampered the XIST-promoted EMT. The results from the luciferase reporter assays confirmed that miR-34a directly targets XIST and suggested that XIST regulates cell proliferation, invasiveness, and apoptosis in PC by sponging miR-34a. Conclusions: XIST promotes TGF-β1-induced EMT by regulating the miR-34a–YAP–EGFR axis in PC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-04-23T07:00:00Z
      DOI: 10.1139/bcb-2018-0274
  • Propofol promotes apoptosis of colorectal cancer cells via alleviating the
           suppression of lncRNA HOXA11-AS on miRNA let-7i
    • Authors: Yan-Ling Ren, Wei Zhang
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      To date, surgical resection is the mainstay for the treatment of colorectal cancer (CRC). Propofol (2,6-diisopropylphenol), one of the most commonly used intravenous anaesthetic agents, has been reported to be involved in modulating the malignancy of a variety of human cancers. However, the underlying mechanisms remain poorly understood. In this study, using a cell counting kit (CCK-8), flow cytometry, and caspase-3 cleavage assays, we found that propofol promoted cell apoptosis and inhibited cell proliferation in both Colo205 and SW620 cells, through the down-regulation of HOXA11-AS and up-regulation of let-7i. Moreover, gain-of-function studies of HOXA11-AS or loss-of-function studies of let-7i also revealed a negative correlation between HOXA11-AS and let-7i in propofol-mediated biological functions of CRC cells. Furthermore, our mechanistic experiments revealed that HOXA11-AS acts as a molecular sponge for let-7i, thereby regulating the expression of ABCC10. We investigate the theory that propofol suppresses colorectal cancer tumorigenesis by modulating the HOXA11-AS–let-7i–ABCC10 regulatory network, indicating the potential for propofol to control CRC development.
      Citation: Biochemistry and Cell Biology
      PubDate: 2019-04-23T07:00:00Z
      DOI: 10.1139/bcb-2018-0235
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