Publisher: BMC (Biomed Central)   (Total: 308 journals)

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Showing 1 - 200 of 308 Journals sorted alphabetically
Acta Neuropathologica Communications     Open Access   (Followers: 1, SJR: 2.683, CiteScore: 5)
Acta Veterinaria Scandinavica     Open Access   (Followers: 4, SJR: 0.655, CiteScore: 1)
Addiction Science & Clinical Practice     Open Access   (Followers: 11, SJR: 1.224, CiteScore: 3)
Advances in Simulation     Open Access   (Followers: 7)
Agriculture & Food Security     Open Access   (Followers: 29, SJR: 0.575, CiteScore: 2)
AIDS Research and Therapy     Open Access   (Followers: 16, SJR: 1.08, CiteScore: 2)
Algorithms for Molecular Biology     Open Access   (Followers: 4, SJR: 1.333, CiteScore: 2)
Allergy, Asthma and Clinical Immunology     Open Access   (Followers: 29, SJR: 0.732, CiteScore: 2)
Alzheimer's Research & Therapy     Open Access   (Followers: 5, SJR: 2.449, CiteScore: 6)
Animal Biotelemetry     Open Access   (Followers: 2, SJR: 1.067, CiteScore: 2)
Animal Diseases     Open Access  
Animal Microbiome     Open Access   (Followers: 3)
Annals of Clinical Microbiology and Antimicrobials     Open Access   (Followers: 13, SJR: 1.104, CiteScore: 3)
Annals of General Psychiatry     Open Access   (Followers: 28, SJR: 0.784, CiteScore: 2)
Annals of Occupational and Environmental Medicine     Open Access   (Followers: 15, SJR: 0.452, CiteScore: 1)
Annals of Surgical Innovation and Research     Open Access   (Followers: 3, SJR: 0.328, CiteScore: 1)
Antimicrobial Resistance and Infection Control     Open Access   (Followers: 13, SJR: 1.573, CiteScore: 3)
Archives of Physiotherapy     Open Access   (Followers: 20)
Archives of Public Health     Open Access   (Followers: 13, SJR: 1.244, CiteScore: 3)
Arthritis Research & Therapy     Open Access   (Followers: 18, SJR: 2.154, CiteScore: 4)
Asthma Research and Practice     Open Access   (Followers: 2)
Basic and Clinical Andrology     Open Access   (SJR: 0.564, CiteScore: 2)
Behavioral and Brain Functions     Open Access   (Followers: 5, SJR: 0.986, CiteScore: 3)
Big Data Analytics     Open Access   (Followers: 34)
BioData Mining     Open Access   (Followers: 5, SJR: 0.982, CiteScore: 2)
Bioelectronic Medicine     Open Access   (Followers: 1)
Biological Procedures Online     Open Access   (SJR: 1.352, CiteScore: 4)
Biological Research     Open Access   (Followers: 1, SJR: 0.654, CiteScore: 2)
Biology Direct     Open Access   (Followers: 10, SJR: 1.694, CiteScore: 3)
Biology of Sex Differences     Open Access   (Followers: 2, SJR: 1.902, CiteScore: 4)
Biomarker Research     Open Access   (Followers: 3)
Biomaterials Research     Open Access   (Followers: 6, SJR: 0.735, CiteScore: 3)
Biomedical Dermatology     Open Access  
BioMedical Engineering OnLine     Open Access   (Followers: 7, SJR: 0.542, CiteScore: 2)
BioPsychoSocial Medicine     Open Access   (Followers: 9, SJR: 0.416, CiteScore: 1)
Biotechnology for Biofuels     Open Access   (Followers: 9, SJR: 1.899, CiteScore: 6)
BMC Anesthesiology     Open Access   (Followers: 18, SJR: 0.807, CiteScore: 2)
BMC Biochemistry     Open Access   (Followers: 15, SJR: 0.708, CiteScore: 2)
BMC Bioinformatics     Open Access   (Followers: 216, SJR: 1.479, CiteScore: 2)
BMC Biology     Open Access   (Followers: 63, SJR: 3.842, CiteScore: 5)
BMC Biomedical Engineering     Open Access  
BMC Biophysics     Open Access   (Followers: 4, SJR: 0.682, CiteScore: 2)
BMC Biotechnology     Open Access   (Followers: 17, SJR: 1.012, CiteScore: 3)
BMC Cancer     Open Access   (Followers: 34, SJR: 1.464, CiteScore: 3)
BMC Cardiovascular Disorders     Open Access   (Followers: 25, SJR: 0.909, CiteScore: 2)
BMC Chemical Engineering     Open Access  
BMC Clinical Pathology     Open Access   (Followers: 8, SJR: 1.141, CiteScore: 3)
BMC Complementary Medicine and Therapies     Open Access   (Followers: 24, SJR: 0.858, CiteScore: 3)
BMC Dermatology     Open Access   (Followers: 14, SJR: 0.796, CiteScore: 2)
BMC Developmental Biology     Open Access   (Followers: 14, SJR: 1.43, CiteScore: 2)
BMC Ear, Nose and Throat Disorders     Open Access   (Followers: 1, SJR: 0.653, CiteScore: 2)
BMC Ecology     Open Access   (Followers: 24, SJR: 1.076, CiteScore: 2)
BMC Emergency Medicine     Open Access   (Followers: 25, SJR: 0.572, CiteScore: 1)
BMC Endocrine Disorders     Open Access   (Followers: 7, SJR: 0.965, CiteScore: 2)
BMC Energy     Open Access  
BMC Evolutionary Biology     Open Access   (Followers: 74, SJR: 1.656, CiteScore: 3)
BMC Family Practice     Open Access   (Followers: 16, SJR: 1.137, CiteScore: 2)
BMC Gastroenterology     Open Access   (Followers: 13, SJR: 1.231, CiteScore: 3)
BMC Genetics     Open Access   (Followers: 32, SJR: 1.16, CiteScore: 3)
BMC Genomics     Open Access   (Followers: 92, SJR: 2.11, CiteScore: 4)
BMC Geriatrics     Open Access   (Followers: 19, SJR: 1.257, CiteScore: 3)
BMC Health Services Research     Open Access   (Followers: 20, SJR: 1.151, CiteScore: 2)
BMC Hematology     Open Access   (Followers: 7, SJR: 0.545, CiteScore: 1)
BMC Immunology     Open Access   (Followers: 11, SJR: 0.993, CiteScore: 3)
BMC Infectious Diseases     Open Access   (Followers: 21, SJR: 1.576, CiteScore: 3)
BMC Intl. Health and Human Rights     Open Access   (Followers: 8, SJR: 1.006, CiteScore: 2)
BMC Materials     Open Access   (Followers: 1)
BMC Medical Education     Open Access   (Followers: 50, SJR: 0.765, CiteScore: 2)
BMC Medical Ethics     Open Access   (Followers: 25, SJR: 1.016, CiteScore: 2)
BMC Medical Genetics     Open Access   (Followers: 9, SJR: 1.109, CiteScore: 2)
BMC Medical Genomics     Open Access   (Followers: 5, SJR: 1.688, CiteScore: 3)
BMC Medical Imaging     Open Access   (Followers: 11, SJR: 0.536, CiteScore: 2)
BMC Medical Informatics and Decision Making     Open Access   (Followers: 25, SJR: 0.812, CiteScore: 2)
BMC Medical Physics     Open Access   (Followers: 8)
BMC Medical Research Methodology     Open Access   (Followers: 8, SJR: 2.221, CiteScore: 3)
BMC Medicine     Open Access   (Followers: 15, SJR: 4.219, CiteScore: 7)
BMC Microbiology     Open Access   (Followers: 17, SJR: 1.242, CiteScore: 3)
BMC Molecular and Cell Biology     Open Access   (Followers: 50, SJR: 1.277, CiteScore: 3)
BMC Molecular Biology     Open Access   (Followers: 207, SJR: 1.216, CiteScore: 2)
BMC Musculoskeletal Disorders     Open Access   (Followers: 30, SJR: 0.951, CiteScore: 2)
BMC Nephrology     Open Access   (Followers: 10, SJR: 1.098, CiteScore: 3)
BMC Neurology     Open Access   (Followers: 23, SJR: 1.006, CiteScore: 2)
BMC Neuroscience     Open Access   (Followers: 18, SJR: 1.12, CiteScore: 2)
BMC Nursing     Open Access   (Followers: 31, SJR: 0.766, CiteScore: 2)
BMC Nutrition     Open Access   (Followers: 12)
BMC Obesity     Open Access   (Followers: 9)
BMC Ophthalmology     Open Access   (Followers: 22, SJR: 0.921, CiteScore: 2)
BMC Oral Health     Open Access   (Followers: 7, SJR: 0.867, CiteScore: 2)
BMC Palliative Care     Open Access   (Followers: 39, SJR: 1.105, CiteScore: 2)
BMC Pediatrics     Open Access   (Followers: 21, SJR: 1.278, CiteScore: 2)
BMC Pharmacology     Open Access   (Followers: 3)
BMC Pharmacology & Toxicology     Open Access   (Followers: 8, SJR: 0.785, CiteScore: 2)
BMC Physiology     Open Access   (Followers: 4, SJR: 0.936, CiteScore: 2)
BMC Plant Biology     Open Access   (Followers: 20, SJR: 1.887, CiteScore: 4)
BMC Pregnancy and Childbirth     Open Access   (Followers: 24, SJR: 1.427, CiteScore: 3)
BMC Proceedings     Full-text available via subscription   (Followers: 2, SJR: 0.302, CiteScore: 1)
BMC Psychiatry     Open Access   (Followers: 41, SJR: 1.346, CiteScore: 3)
BMC Psychology     Open Access   (Followers: 22, SJR: 0.817, CiteScore: 2)
BMC Public Health     Open Access   (Followers: 229, SJR: 1.337, CiteScore: 3)
BMC Pulmonary Medicine     Open Access   (Followers: 7, SJR: 1.373, CiteScore: 3)
BMC Research Notes     Open Access   (Followers: 4, SJR: 0.691, CiteScore: 2)
BMC Rheumatology     Open Access   (Followers: 5)
BMC Sports Science, Medicine and Rehabilitation     Open Access   (Followers: 36, SJR: 0.926, CiteScore: 2)
BMC Structural Biology     Open Access   (Followers: 8, SJR: 1.024, CiteScore: 2)
BMC Surgery     Open Access   (Followers: 10, SJR: 0.693, CiteScore: 2)
BMC Systems Biology     Open Access   (Followers: 16, SJR: 1.109, CiteScore: 2)
BMC Urology     Open Access   (Followers: 14, SJR: 0.853, CiteScore: 2)
BMC Veterinary Research     Open Access   (Followers: 20, SJR: 0.934, CiteScore: 2)
BMC Women's Health     Open Access   (Followers: 16, SJR: 0.931, CiteScore: 2)
BMC Zoology     Open Access   (Followers: 1)
BMJ Evidence-Based Medicine     Hybrid Journal   (Followers: 9)
Borderline Personality Disorder and Emotion Dysregulation     Open Access   (Followers: 10)
Breast Cancer Research     Open Access   (Followers: 22, SJR: 3.026, CiteScore: 6)
Burns & Trauma     Open Access   (Followers: 14)
CABI Agriculture and Bioscience     Open Access   (Followers: 2)
Cancer & Metabolism     Open Access   (Followers: 7)
Cancer Cell Intl.     Open Access   (Followers: 7, SJR: 1.13, CiteScore: 3)
Cancer Communications     Open Access  
Cancer Convergence     Open Access   (Followers: 1)
Cancer Imaging     Open Access   (Followers: 3, SJR: 1.012, CiteScore: 3)
Cancer Nanotechnology     Open Access   (Followers: 2, SJR: 1.168, CiteScore: 4)
Cancers of the Head & Neck     Open Access   (Followers: 3)
Carbon Balance and Management     Open Access   (Followers: 5, SJR: 0.977, CiteScore: 2)
Cardio-Oncology     Open Access  
Cardiovascular Diabetology     Open Access   (Followers: 10, SJR: 2.157, CiteScore: 5)
Cardiovascular Ultrasound     Open Access   (Followers: 6, SJR: 0.812, CiteScore: 2)
Cell Communication and Signaling     Open Access   (Followers: 3, SJR: 2.211, CiteScore: 4)
Cell Division     Open Access   (Followers: 1, SJR: 2.445, CiteScore: 4)
Cellular & Molecular Biology Letters     Hybrid Journal   (Followers: 3)
Cerebellum & Ataxias     Open Access   (Followers: 1)
Chemistry Central J.     Open Access   (Followers: 5, SJR: 0.607, CiteScore: 3)
Child and Adolescent Psychiatry and Mental Health     Open Access   (Followers: 30, SJR: 0.901, CiteScore: 2)
Chinese Medicine     Open Access   (Followers: 2, SJR: 0.57, CiteScore: 2)
Chinese Neurosurgical J.     Open Access  
Chiropractic & Manual Therapies     Open Access   (Followers: 5, SJR: 0.599, CiteScore: 2)
Clinical and Molecular Allergy     Open Access   (Followers: 5, SJR: 0.933, CiteScore: 3)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 23)
Clinical Epigenetics     Open Access   (Followers: 11, SJR: 2.435, CiteScore: 5)
Clinical Hypertension     Open Access   (Followers: 5)
Conflict and Health     Open Access   (Followers: 8, SJR: 1.851, CiteScore: 3)
Contraception and Reproductive Medicine     Open Access   (Followers: 2)
COPD Research and Practice     Open Access   (Followers: 1, SJR: 0.755, CiteScore: 2)
Cost Effectiveness and Resource Allocation     Open Access   (Followers: 5, SJR: 0.888, CiteScore: 2)
Critical Care     Open Access   (Followers: 82, SJR: 2.48, CiteScore: 5)
Current Opinion in Molecular Therapeutics     Full-text available via subscription   (Followers: 13)
Diabetology & Metabolic Syndrome     Open Access   (Followers: 7, SJR: 0.943, CiteScore: 2)
Diagnostic and Prognostic Research     Open Access  
Diagnostic Pathology     Open Access   (Followers: 14, SJR: 0.818, CiteScore: 2)
Disaster and Military Medicine     Open Access   (Followers: 5)
Emerging Themes in Epidemiology     Open Access   (Followers: 14, SJR: 1.003, CiteScore: 2)
Energy, Sustainability and Society     Open Access   (Followers: 18, SJR: 0.607, CiteScore: 2)
Environmental Health     Open Access   (Followers: 15, SJR: 1.662, CiteScore: 4)
Environmental Health and Preventive Medicine     Open Access   (Followers: 4, SJR: 0.5, CiteScore: 1)
Environmental Microbiome     Open Access   (SJR: 0.768, CiteScore: 2)
Epigenetics & Chromatin     Open Access   (Followers: 8, SJR: 3.767, CiteScore: 5)
European J. of Medical Research     Open Access   (Followers: 2, SJR: 0.55, CiteScore: 1)
European Review of Aging and Physical Activity     Open Access   (Followers: 12, SJR: 1.308, CiteScore: 4)
Experimental & Translational Stroke Medicine     Open Access   (Followers: 10, SJR: 0.98, CiteScore: 3)
Experimental Hematology & Oncology     Open Access   (Followers: 6, SJR: 0.842, CiteScore: 2)
ExRNA     Open Access  
Eye and Vision     Open Access   (Followers: 1)
Fertility Research and Practice     Open Access   (Followers: 2)
Fibrogenesis & Tissue Repair     Open Access   (SJR: 1.531, CiteScore: 4)
Fisheries and Aquatic Sciences     Open Access   (Followers: 3, SJR: 0.199, CiteScore: 0)
Fluids and Barriers of the CNS     Open Access   (Followers: 3, SJR: 2.054, CiteScore: 5)
Frontiers in Zoology     Open Access   (Followers: 12, SJR: 1.597, CiteScore: 3)
Genes and Environment     Open Access   (Followers: 1, SJR: 0.516, CiteScore: 1)
Genetics Selection Evolution     Open Access   (Followers: 7, SJR: 1.745, CiteScore: 4)
Genome Biology     Open Access   (Followers: 41)
Genome Medicine     Open Access   (Followers: 7, SJR: 4.537, CiteScore: 7)
Global Health Research and Policy     Open Access   (Followers: 4)
Globalization and Health     Open Access   (Followers: 9, SJR: 1.262, CiteScore: 2)
Gut Pathogens     Full-text available via subscription   (Followers: 6, SJR: 1.066, CiteScore: 3)
Gynecologic Oncology Research and Practice     Open Access   (Followers: 1)
Harm Reduction J.     Open Access   (SJR: 1.445, CiteScore: 3)
Head & Face Medicine     Open Access   (Followers: 1, SJR: 0.62, CiteScore: 2)
Health and Quality of Life Outcomes     Open Access   (Followers: 15, SJR: 1.069, CiteScore: 3)
Health Research Policy and Systems     Open Access   (Followers: 16, SJR: 1.11, CiteScore: 2)
Hereditary Cancer in Clinical Practice     Open Access   (Followers: 2, SJR: 0.848, CiteScore: 2)
Hereditas     Open Access   (Followers: 1, SJR: 0.278, CiteScore: 1)
Human Genomics     Open Access   (Followers: 3, SJR: 1.501, CiteScore: 3)
Human Resources for Health     Open Access   (Followers: 12, SJR: 1.301, CiteScore: 2)
Immunity & Ageing     Open Access   (Followers: 10, SJR: 1.218, CiteScore: 3)
Implementation Science     Open Access   (Followers: 23, SJR: 2.443, CiteScore: 4)
Implementation Science Communications     Open Access   (Followers: 6)
Infectious Agents and Cancer     Open Access   (SJR: 0.855, CiteScore: 2)
Infectious Diseases of Poverty     Open Access   (Followers: 3, SJR: 1.212, CiteScore: 3)
Inflammation and Regeneration     Open Access   (Followers: 2)
Intl. Breastfeeding J.     Open Access   (Followers: 26, SJR: 0.913, CiteScore: 3)
Intl. J. for Equity in Health     Open Access   (Followers: 9, SJR: 1.04, CiteScore: 2)
Intl. J. of Behavioral Nutrition and Physical Activity     Open Access   (Followers: 32, SJR: 2.626, CiteScore: 6)
Intl. J. of Health Geographics     Open Access   (Followers: 9, SJR: 1.385, CiteScore: 3)
Intl. J. of Mental Health Systems     Open Access   (Followers: 7, SJR: 0.721, CiteScore: 2)
Intl. J. of Pediatric Endocrinology     Open Access   (Followers: 12)
Intl. J. of Retina and Vitreous     Open Access   (Followers: 4)
Investigative Genetics     Open Access   (Followers: 1, SJR: 1.809, CiteScore: 3)
Irish Veterinary J.     Open Access   (Followers: 4, SJR: 0.657, CiteScore: 1)
Israel J. of Health Policy Research     Open Access   (SJR: 0.488, CiteScore: 1)
Italian J. of Pediatrics     Open Access   (Followers: 2, SJR: 0.685, CiteScore: 2)
J. of Angiogenesis Research     Open Access   (Followers: 2)

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Similar Journals
Journal Cover
Cell Division
Journal Prestige (SJR): 2.445
Citation Impact (citeScore): 4
Number of Followers: 1  

  This is an Open Access Journal Open Access journal
ISSN (Print) 1747-1028
Published by BMC (Biomed Central) Homepage  [308 journals]
  • Ral GTPase is essential for actin dynamics and Golgi apparatus
           distribution in mouse oocyte maturation

    • Abstract: Background Ral family is a member of Ras-like GTPase superfamily, which includes RalA and RalB. RalA/B play important roles in many cell biological functions, including cytoskeleton dynamics, cell division, membrane transport, gene expression and signal transduction. However, whether RalA/B involve into the mammalian oocyte meiosis is still unclear. This study aimed to explore the roles of RalA/B during mouse oocyte maturation. Results Our results showed that RalA/B expressed at all stages of oocyte maturation, and they were enriched at the spindle periphery area after meiosis resumption. The injection of RalA/B siRNAs into the oocytes significantly disturbed the polar body extrusion, indicating the essential roles of RalA/B for oocyte maturation. We observed that in the RalA/B knockdown oocytes the actin filament fluorescence intensity was significantly increased at the both cortex and cytoplasm, and the chromosomes were failed to locate near the cortex, indicating that RalA/B regulate actin dynamics for spindle migration in mouse oocytes. Moreover, we also found that the Golgi apparatus distribution at the spindle periphery was disturbed after RalA/B depletion. Conclusions In summary, our results indicated that RalA/B affect actin dynamics for chromosome positioning and Golgi apparatus distribution in mouse oocytes.
      PubDate: 2021-06-10
       
  • Mitotic arrest affects clustering of tumor cells

    • Abstract: Background Cancer cell aggregation is a key process involved in the formation of tumor cell clusters. It has recently been shown that clusters of circulating tumor cells (CTCs) have an increased metastatic potential compared to isolated circulating tumor cells. Several widely used chemotherapeutic agents that target the cytoskeleton microtubules and cause cell cycle arrest at mitosis have been reported to modulate CTC number or the size of CTC clusters. Results In this study, we investigated in vitro the impact of mitotic arrest on the ability of breast tumor cells to form clusters. By using live imaging and quantitative image analysis, we found that MCF-7 cancer cell aggregation is compromised upon incubation with paclitaxel or vinorelbine, two chemotherapeutic drugs that target microtubules. In line with these results, we observed that MCF-7 breast cancer cells experimentally synchronized and blocked in metaphase aggregated poorly and formed loose clusters. To monitor clustering at the single-cell scale, we next developed and validated an in vitro assay based on live video-microscopy and custom-designed micro-devices. The study of cluster formation from MCF-7 cells that express the fluorescent marker LifeAct-mCherry using this new assay allowed showing that substrate anchorage-independent clustering of MCF-7 cells was associated with the formation of actin-dependent highly dynamic cell protrusions. Metaphase-synchronized and blocked cells did not display such protrusions, and formed very loose clusters that failed to compact. Conclusions Altogether, our results suggest that mitotic arrest induced by microtubule-targeting anticancer drugs prevents cancer cell clustering and therefore, could reduce the metastatic potential of circulating tumor cells.
      PubDate: 2021-01-29
       
  • Microarray expression profile of mRNAs and long noncoding RNAs and the
           potential role of PFK-1 in infantile hemangioma

    • Abstract: Background Infantile hemangioma (IH) is the most common benign tumor in children. Long noncoding RNAs (lncRNAs) play a critical role in tumorigenesis. However, the expression levels and biological functions of lncRNAs in IH have not been well-studied. This study aimed to analyze the expression profile of lncRNAs and mRNAs in proliferating and involuting IHs. Methods The expression profiles of lncRNAs and mRNAs in proliferating and involuting IHs were identified by microarray analysis. Subsequently, detailed bioinformatics analyses were performed. Finally, quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) analyses were conducted to validate the microarray results. Results In total, 146 differentially expressed (DE) lncRNAs and 374 DE mRNAs were identified. The DE mRNAs were enriched mostly in angiogenesis-related biological processes (BPs) and pathways by bioinformatics analysis. In addition, metabolism-related BPs (e.g., “glycogen biosynthetic process” and “metabolic process”) and pathways (e.g., “oxidative phosphorylation”) were identified. A lncRNA-mRNA co-expression network was constructed from 42 DE lncRNAs and 217 DE mRNAs. Twelve lncRNAs were predicted to have cis-regulated target genes. The microarray analysis results were validated by qRT-PCR using 5 randomly selected lncRNAs and 13 mRNAs. The IHC results revealed that both LOXL2 and FPK-1 exhibited higher protein expression levels in proliferating IH than in involuting IH. Moreover, inhibition of PFK-1 could suppress hemangioma-derived endothelial cell proliferation and migration, induce cell arrest, and reduce glucose uptake and lactate and ATP production. Conclusions The findings suggest that the identified DE lncRNAs and mRNAs may be associated with the pathogenesis of IH. The data presented herein can improve our understanding of IH development and provide direction for further studies investigating the mechanism underlying IH.
      PubDate: 2021-01-11
       
  • Chromosomal aberration arises during somatic reprogramming to pluripotent
           stem cells

    • Abstract: Background Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) has opened new therapeutic possibilities. However, karyotypic abnormalities detected in iPSCs compromised their utility, especially chromosomal aberrations found at early passages raised serious safety concerns. The mechanism underlying the chromosomal abnormality in early-passage iPSCs is not known. Methods Human dermal fibroblasts (HDFs) were stimulated with KMOS (KLF4, cMYC, OCT4 and SOX2) proteins to enhance their proliferative capacity and many vigorous clones were obtained. Clonal reprogramming was carried out by KMOS mRNAs transfection to confirm the ‘chromosomal mutagenicity’ of reprogramming process. Subculturing was performed to examine karyotypic stability of iPSCs after the re-establishment of stemness. And antioxidant N-acetyl-cysteine (NAC) was added to the culture medium for further confirmming the mutagenicity in the first few days of reprogramming. Results Chromosomal aberrations were found in a small percentage of newly induced iPS clones by reprogramming transcription factors. Clonal reprogramming ruled out the aberrant chromosomes inherited from rare karyotypically abnormal parental cell subpopulation. More importantly, the antioxidant NAC effectively reduced the occurrence of chromosomal aberrations at the early stage of reprogramming. Once iPS cell lines were established, they restored karyotypic stability in subsequent subculturing. Conclusions Our results provided the first line of evidence for the ‘chromosomal mutagenicity’ of reprogramming process.
      PubDate: 2020-11-03
       
  • XMU-MP-1 induces growth arrest in a model human mini-organ and antagonises
           cell cycle-dependent paclitaxel cytotoxicity

    • Abstract: Background XMU-MP-1 is an inhibitor of the Hippo pathway kinases MST1/2 and has been shown to promote the downstream activation of the pro-proliferative, pro-regenerative and anti-apoptotic transcriptional regulator YAP1. We tested whether XMU-MP-1 can activate YAP1 in a model human mini-organ, namely the hair follicle, to determine whether it can be pharmacologically exploited to promote regeneration in the hair follicle as a novel strategy to treat pathological hair loss disorders. Results XMU-MP-1 treatment inhibited MOB1 phosphorylation but did not increase active YAP1 in the hair follicle. Rather than promote proliferation, XMU-MP-1 serendipitously decreased the number of Ki-67+, EdU+ and phospho histone H3+ hair matrix keratinocytes and antagonised the cytotoxic effects of paclitaxel. Conclusions XMU-MP-1 perturbs epithelial cell cycle progression in a model human mini-organ. This may arise as an off-target effect, especially when XMU-MP-1 has been described to strongly inhibit 21 additional kinases beyond MST1/2. Therefore, whilst these effects may be dependent on tissue context, researchers should exercise caution when interpreting the effects of XMU-MP-1, especially in tissues with actively proliferating cell populations.
      PubDate: 2020-09-17
       
  • Caffeine as a tool for investigating the integration of Cdc25
           phosphorylation, activity and ubiquitin-dependent degradation in
           Schizosaccharomyces pombe

    • Abstract: The evolutionarily conserved Cdc25 phosphatase is an essential protein that removes inhibitory phosphorylation moieties on the mitotic regulator Cdc2. Together with the Wee1 kinase, a negative regulator of Cdc2 activity, Cdc25 is thus a central regulator of cell cycle progression in Schizosaccharomyces pombe. The expression and activity of Cdc25 is dependent on the activity of the Target of Rapamycin Complex 1 (TORC1). TORC1 inhibition leads to the activation of Cdc25 and repression of Wee1, leading to advanced entry into mitosis. Withdrawal of nitrogen leads to rapid Cdc25 degradation via the ubiquitin- dependent degradation pathway by the Pub1 E3- ligase. Caffeine is believed to mediate the override of DNA damage checkpoint signalling, by inhibiting the activity of the ataxia telangiectasia mutated (ATM)/Rad3 homologues. This model remains controversial, as TORC1 appears to be the preferred target of caffeine in vivo. Recent studies suggest that caffeine induces DNA damage checkpoint override by inducing the nuclear accumulation of Cdc25 in S. pombe. Caffeine may thus modulate Cdc25 activity and stability via inhibition of TORC1. A clearer understanding of the mechanisms by which caffeine stabilises Cdc25, may provide novel insights into how TORC1 and DNA damage signalling is integrated.
      PubDate: 2020-06-29
       
  • EZH2-inhibitor DZNep enhances apoptosis of renal tubular epithelial cells
           in presence and absence of cisplatin

    • Abstract: Background The enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase and induces the trimethylation of histone H3 lysine 27 (H3K27me3) in the promoter of many key genes; EZH2 acts as a transcriptional repressor and is an epigenetic regulator for several cancers. However, the role of EZH2 in nonneoplastic diseases, such as kidney diseases, is unknown and has been investigated. Materials and method NRK-52E cells were treated with DZNep, a potent inhibitor of EZH2, with different concentrations and for different times to evaluate the apoptosis level of NRK-52E cells by Western blot and Flow cytometry analysis. The binding of EZH2 to the Deptor promoter was determined by ChIP assay. Results The inhibition of EZH2 with 3-deazaneplanocin A (DZNep), a specific inhibitor of EZH2, led to the apoptosis of NRK-52E cells and the inhibition of mTORC1 and mTORC2 activity. A ChIP assay demonstrated that EZH2 bound the promoter region of Deptor, an endogenous inhibitor of mTORC1 and mTORC2, and regulated the transcription of Deptor by modulating H3K27me3 in its promoter region. Further experiments were performed to examine the effects of EZH2 inhibition on cisplatin-induced injured cells. Cisplatin induced the activation of mTORC1 and mTORC2 and apoptosis in NRK-52E cells, and DZNep inhibited mTORC1 and mTORC2 activity and aggravated cell apoptosis. Conclusions These data suggested that EZH2 inhibition increased the transcription of Deptor by modifying H3K27me3 in its promoter region, subsequently inhibited mTORC1 and mTORC2 activities, downregulated the expression of apoptosis suppressor genes, and finally led to apoptosis in renal tubular cells. The inhibition of EZH2 aggravated the cisplatin-induced injury in renal tubular cells by inactivating the mTOR complexes. The present study provides new insight into renal protection and suggests that EZH2 might be a target.
      PubDate: 2020-05-25
       
  • The G2-to-M transition from a phosphatase perspective: a new vision of the
           meiotic division

    • Abstract: Cell division is orchestrated by the phosphorylation and dephosphorylation of thousands of proteins. These post-translational modifications underlie the molecular cascades converging to the activation of the universal mitotic kinase, Cdk1, and entry into cell division. They also govern the structural events that sustain the mechanics of cell division. While the role of protein kinases in mitosis has been well documented by decades of investigations, little was known regarding the control of protein phosphatases until the recent years. However, the regulation of phosphatase activities is as essential as kinases in controlling the activation of Cdk1 to enter M-phase. The regulation and the function of phosphatases result from post-translational modifications but also from the combinatorial association between conserved catalytic subunits and regulatory subunits that drive their substrate specificity, their cellular localization and their activity. It now appears that sequential dephosphorylations orchestrated by a network of phosphatase activities trigger Cdk1 activation and then order the structural events necessary for the timely execution of cell division. This review discusses a series of recent works describing the important roles played by protein phosphatases for the proper regulation of meiotic division. Many breakthroughs in the field of cell cycle research came from studies on oocyte meiotic divisions. Indeed, the meiotic division shares most of the molecular regulators with mitosis. The natural arrests of oocytes in G2 and in M-phase, the giant size of these cells, the variety of model species allowing either biochemical or imaging as well as genetics approaches explain why the process of meiosis has served as an historical model to decipher signalling pathways involved in the G2-to-M transition. The review especially highlights how the phosphatase PP2A-B55δ critically orchestrates the timing of meiosis resumption in amphibian oocytes. By opposing the kinase PKA, PP2A-B55δ controls the release of the G2 arrest through the dephosphorylation of their substrate, Arpp19. Few hours later, the inhibition of PP2A-B55δ by Arpp19 releases its opposing kinase, Cdk1, and triggers M-phase. In coordination with a variety of phosphatases and kinases, the PP2A-B55δ/Arpp19 duo therefore emerges as the key effector of the G2-to-M transition.
      PubDate: 2020-05-25
       
  • Toll signaling promotes JNK-dependent apoptosis in Drosophila

    • Abstract: Background Apoptosis plays pivotal roles in organ development and tissue homeostasis, with its major function to remove unhealthy cells that may compromise the fitness of the organism. Toll signaling, with the ancient evolutionary origin, regulates embryonic dorsal–ventral patterning, axon targeting and degeneration, and innate immunity. Using Drosophila as a genetic model, we characterized the role of Toll signaling in apoptotic cell death. Results We found that gain of Toll signaling is able to trigger caspase-dependent cell death in development. In addition, JNK activity is required for Toll-induced cell death. Furthermore, ectopic Toll expression induces the activation of JNK pathway. Moreover, physiological activation of Toll signaling is sufficient to produce JNK-dependent cell death. Finally, Toll signaling activates JNK-mediated cell death through promoting ROS production. Conclusions As Toll pathway has been evolutionarily conserved from Drosophila to human, this study may shed light on the mechanism of mammalian Toll-like receptors (TLRs) signaling in apoptotic cell death.
      PubDate: 2020-03-10
       
  • Kinesin-5 Eg5 is essential for spindle assembly and chromosome alignment
           of mouse spermatocytes

    • Abstract: Background Microtubule organization is essential for bipolar spindle assembly and chromosome segregation, which contribute to genome stability. Kinesin-5 Eg5 is known to be a crucial regulator in centrosome separation and spindle assembly in mammalian somatic cells, however, the functions and mechanisms of Eg5 in male meiotic cell division remain largely unknown. Results In this study, we have found that Eg5 proteins are expressed in mouse spermatogonia, spermatocytes and spermatids. After Eg5 inhibition by specific inhibitors Monastrol, STLC and Dimethylenastron, the meiotic spindles of dividing spermatocytes show spindle collapse and the defects in bipolar spindle formation. We demonstrate that Eg5 regulates spindle bipolarity and the maintenance of meiotic spindles in meiosis. Eg5 inhibition leads to monopolar spindles, spindle abnormalities and chromosome misalignment in cultured GC-2 spd cells. Furthermore, Eg5 inhibition results in the decrease of the spermatids and the abnormalities in mature sperms. Conclusions Our results have revealed an important role of kinesin-5 Eg5 in male meiosis and the maintenance of male fertility. We demonstrate that Eg5 is crucial for bipolar spindle assembly and chromosome alignment in dividing spermatocytes. Our data provide insights into the functions of Eg5 in meiotic spindle assembly of dividing spermatocytes.
      PubDate: 2020-03-06
       
  • IGFBP5 increases cell invasion and inhibits cell proliferation by EMT and
           Akt signaling pathway in Glioblastoma multiforme cells

    • Abstract: Background Recurrence of Glioblastoma multiforme (GBM) seems to be the rule despite combination therapies. Cell invasion and cell proliferation are major reasons for recurrence of GBM. And insulin-like growth factor binding protein 5 (IGFBP5) is the most conserved of the IGFBPs and is frequently dysregulated in cancers and metastatic tissues. Results By studying the human glioma tissues, we find that IGFBP5 expression associate to the histopathological classification and highly expressed in GBM. Using IGFBP5 mutants we demonstrate that knockdown of IGFBP5 inhibited cell invasion, whereas promoting cell proliferation in GBM cells. Mechanistically, we observed that promoting GBM cell proliferation by inhibiting IGFBP5 was associated with stimulating Akt (Protein kinase B) phosphorylation. However, IGFBP5 promote GBM cell invasion was related to the epithelial-to-mesenchymal transition (EMT). Furthermore, the Chinese Glioma Genome Altas (CGGA) database show that IGFBP5 is significantly increased in recurrent glioma and it predicted worse survival. Conclusions The obtained results indicate that IGFBP5 has two sides in GBM—inhibiting cell proliferation but promoting cell invasion.
      PubDate: 2020-02-27
       
  • A positive feedback loop between EZH2 and NOX4 regulates nucleus pulposus
           cell senescence in age-related intervertebral disc degeneration

    • Abstract: Background The senescence of nucleus pulposus (NP) cells plays a vital role in the pathogenesis of intervertebral disc (IVD) degeneration (IDD). NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce premature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence. The aim of this study was to investigate the roles of EZH2 in NOX4-induced NP cell senescence and a feedback loop between EZH2 and NOX4. Results The down-regulation of EZH2 and the up-regulation of NOX4 and p16 were observed in the degenerative discs of aging rats. EZH2 regulated NP cell senescence via the H3K27me3-p16 pathway. Also, EZH2 regulated the expression of NOX4 in NP cells through the histone H3 lysine 27 trimethylation (H3K27me3) in the promoter of NOX4 gene. Furthermore, NOX4 down-regulated EZH2 expression in NP cells via the canonical Wnt/β-catenin pathway. Conclusions A positive feedback loop between EZH2 and NOX4 is involved in regulating NP cell senescence, which provides a novel insight into the mechanism of IDD and a potential therapeutic target for IDD.
      PubDate: 2020-02-01
       
  • Coupled cycling and regulation of metazoan morphogenesis

    • Abstract: Metazoan animals are characterized by restricted phenotypic heterogeneity (i.e. morphological disparity) of organisms within various species, a feature that contrasts sharply with intra-species morphological diversity observed in the plant kingdom. Robust emergence of morphogenic blueprint in metazoan animals reflects restricted autonomy of individual cells in adoption of fate outcomes such as differentiation. Fates of individual cells are linked to and influenced by fates of neighboring cells at the population level. Such coupling is a common property of all self-organising systems and propels emergence of order from simple interactions between individual cells without supervision by external directing forces. As a consequence of coupling, expected functional relationship between the constituent cells of an organ system is robustly established concurrent with multiple rounds of cell division during morphogenesis. Notably, the molecular regulation of multicellular coupling during morphogenic self-organisation remains largely unexplored. Here, we review the existing literature on multicellular self-organisation with particular emphasis on recent discovery that β-catenin is the key coupling factor that programs emergence of multi-cellular self-organisation by regulating synchronised cycling of individual cells.
      PubDate: 2020-01-27
       
  • Mechanisms for the temporal regulation of substrate ubiquitination by the
           anaphase-promoting complex/cyclosome

    • Abstract: The anaphase-promoting complex/cyclosome (APC/C) is a multi-subunit, multifunctional ubiquitin ligase that controls the temporal degradation of numerous cell cycle regulatory proteins to direct the unidirectional cell cycle phases. Several different mechanisms contribute to ensure the correct order of substrate modification by the APC/C complex. Recent advances in biochemical, biophysical and structural studies of APC/C have provided a deep mechanistic insight into the working of this complex ubiquitin ligase. This complex displays remarkable conformational flexibility in response to various binding partners and post-translational modifications, which together regulate substrate selection and catalysis of APC/C. Apart from this, various features and modifications of the substrates also influence their recognition and affinity to APC/C complex. Ultimately, temporal degradation of substrates depends on the kind of ubiquitin modification received, the processivity of APC/C, and other extrinsic mechanisms. This review discusses our current understanding of various intrinsic and extrinsic mechanisms responsible for ‘substrate ordering’ by the APC/C complex.
      PubDate: 2019-12-23
       
  • The essentiality landscape of cell cycle related genes in human
           pluripotent and cancer cells

    • Abstract: Background Cell cycle regulation is a complex system consisting of growth-promoting and growth-restricting mechanisms, whose coordinated activity is vital for proper division and propagation. Alterations in this regulation may lead to uncontrolled proliferation and genomic instability, triggering carcinogenesis. Here, we conducted a comprehensive bioinformatic analysis of cell cycle-related genes using data from CRISPR/Cas9 loss-of-function screens performed in four cancer cell lines and in human embryonic stem cells (hESCs). Results Cell cycle genes, and in particular S phase and checkpoint genes, are highly essential for the growth of cancer and pluripotent cells. However, checkpoint genes are also found to underlie the differences between the cell cycle features of these cell types. Interestingly, while growth-promoting cell cycle genes overlap considerably between cancer and stem cells, growth-restricting cell cycle genes are completely distinct. Moreover, growth-restricting genes are consistently less frequent in cancer cells than in hESCs. Here we show that most of these genes are regulated by the tumor suppressor gene TP53, which is mutated in most cancer cells. Therefore, the growth-restriction system in cancer cells lacks important factors and does not function properly. Intriguingly, M phase genes are specifically essential for the growth of hESCs and are highly abundant among hESC-enriched genes. Conclusions Our results highlight the differences in cell cycle regulation between cell types and emphasize the importance of conducting cell cycle studies in cells with intact genomes, in order to obtain an authentic representation of the genetic features of the cell cycle.
      PubDate: 2019-12-23
       
  • FGF-induced LHX9 regulates the progression and metastasis of osteosarcoma
           via FRS2/TGF-β/β-catenin pathway

    • Abstract: Background Fibroblast growth factor (FGF) and tumor growth factor-β (TGFβ) have emerged as pivotal regulators during the progression of osteosarcoma (OS). LHX9 is one crucial transcription factor controlled by FGF, however, its function in OS has not been investigated yet. Methods The expression of LHX9, FRS2, BMP4, TGF-beta R1, SMAD2, beta-catenin and metastasis-related proteins was measured by real-time quantitative PCR (RT-qPCR) and Western blot. CCK-8 assay and colony formation assay were employed to determine the proliferation of OS cells, while scratch wound healing assay and transwell assay were used to evaluate their migration and invasion, respectively. In vivo tumor growth and metastasis were determined by subcutaneous or intravenous injection of OS cells into nude mice. Results LHX9 expression was evidently up-regulated in OS tumor tissues and cell lines. Knockdown of LHX9 impaired the proliferation, migration, invasion and metastasis of OS cells. Mechanistically, LHX9 silencing led to the down-regulation of BMP-4, β-catenin and metastasis-related proteins, which was also observed in beta-catenin knockdown OS cells. By contrast, FRS2 knockdown conduced to the up-regulation of LHX9, BMP4, β-catenin and TGF-βR1, while TGF-beta inhibition repressed the expression of LHX9 and metastasis-related proteins. Additionally, let-7c modulates LHX9 and metastasis-related proteins by suppressing TGF-beta R1 expression on transcriptional level. Conclusions This study revealed LHX9 was essential for the proliferation, migration, invasion, and metastasis of OS cells via FGF and TGF-β/β-catenin signaling pathways.
      PubDate: 2019-11-25
       
  • CRY arrests Cop1 to regulate circadian rhythms in mammals

    • Abstract: Cryptochromes (CRYs) are UVA and blue light photoreceptors present in all major evolutionary lineages ranging from cyanobacteria to plants and animals, including mammals. In plants, blue light activates CRYs to induce photomorphogenesis by inhibiting the CRL4Cop1 E3 ligase complex which regulates the degradation of critical transcription factors involved in plant development and growth. However, in mammals, CRYs do not physically interact with Cop1, and of course mammals are not photomorphogenic, leading to the belief that the CRY–Cop1 axis is not conserved in mammals. This belief was recently overturned by Rizzini et al., who showed that although mammalian CRYs do not inhibit Cop1 activity in a light-dependent manner, they antagonize Cop1 activity by displacing Cop1 from CRL4 E3 ligase complex. Because CRYs oscillate, they act in a circadian manner resulting in daily oscillations in Cop1 substrates and the downstream pathways that they regulate. The conserved antagonism of Cop1 by CRY indicates that the CRY–Cop1 axis has an ancient origin, and was repurposed by evolution to regulate photomorphogenesis in plants and circadian rhythms in mammals.
      PubDate: 2019-11-02
       
  • MicroRNAs’ control of cancer cell dormancy

    • Abstract: ‘Dormancy’, in the context of carcinogenesis, is a biological phenomenon of decreased cancer cell proliferation and metabolism. In view of their ability to remain quiescent, cancer cells are able to avoid cell death induced by chemotherapeutic agents, and thereby give rise to tumor relapse at a later stage. Being a dynamic event, the dormant state is controlled by several epigenetic mechanisms, including the action of microRNAs. The present review highlights microRNAs that have been shown to be dysregulated in dormant cancer cells among different tumor types. MicroRNAs accomplish their control of cancer cell quiescence by targeting cell cycle regulators and signaling pathways involved in cell growth maintenance, including the AKT/phosphoinositide 3-kinase (PI3K) pathway. MicroRNAs, as components of intercellular vesicles, enable interactions to occur between cancer cells and cells of the microenvironment, resulting in the cancer cells either acquiring the quiescent state or, oppositely, stimulating them to proliferate. Taken together, the evidence obtained to date has collectively confirmed the involvement of microRNAsin cancer cell dormancy. Modulation of the various processes may enable optimization of the treatment of metastatic tumors.
      PubDate: 2019-10-10
       
  • Correction to: Reactivation of TAp73 tumor suppressor by protoporphyrin
           IX, a metabolite of aminolevulinic acid, induces apoptosis in TP
           53-deficient cancer cells

    • Abstract: The authors note a correction to the article [1]. Figure 1d of the original article has an error. The pcDNA3/Ctrl and the pcDNA3-TAp73a/DMSO wells are duplicated. This article presents the corrected version of Fig. 1.
      PubDate: 2019-08-29
       
  • Septin and Ras regulate cytokinetic abscission in detached cells

    • Abstract: Background Integrin-mediated adhesion is normally required for cytokinetic abscission, and failure in the process can generate potentially oncogenic tetraploid cells. Here, detachment-induced formation of oncogenic tetraploid cells was analyzed in non-transformed human BJ fibroblasts and BJ expressing SV40LT (BJ-LT) ± overactive HRas. Results In contrast to BJ and BJ-LT cells, non-adherent BJ-LT-Ras cells recruited ALIX and CHMP4B to the midbody and divided. In detached BJ and BJ-LT cells regression of the cytokinetic furrow was suppressed by intercellular bridge-associated septin; after re-adhesion these cells divided by cytofission, however, some cells became bi-nucleated because of septin reorganization and furrow regression. Adherent bi-nucleated BJ cells became senescent in G1 with p21 accumulation in the nucleus, apparently due to p53 activation since adherent bi-nucleated BJ-LT cells passed through next cell cycle and divided into mono-nucleated tetraploids; the two centrosomes present in bi-nucleated BJ cells fused after furrow regression, pointing to the PIDDosome pathway as a possible mechanism for the p53 activation. Conclusions Several mechanisms prevent detached normal cells from generating tumor-causing tetraploid cells unless they have a suppressed p53 response by viruses, mutation or inflammation. Importantly, activating Ras mutations promote colony growth of detached transformed cells by inducing anchorage-independent cytokinetic abscission in single cells.
      PubDate: 2019-08-21
       
 
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