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Showing 201 - 310 of 310 Journals sorted alphabetically
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. for ImmunoTherapy of Cancer     Open Access   (Followers: 6, SJR: 2.798, CiteScore: 6)
J. of Angiogenesis Research     Open Access   (Followers: 2)
J. of Animal Science and Biotechnology     Open Access   (Followers: 4, SJR: 1.228, CiteScore: 3)
J. of Animal Science and Technology     Open Access   (Followers: 2)
J. of Biological Engineering     Open Access   (Followers: 3, SJR: 1.34, CiteScore: 4)
J. of Biological Research - Thessaloniki     Open Access   (SJR: 0.32, CiteScore: 2)
J. of Biomedical Semantics     Open Access   (Followers: 2, SJR: 0.952, CiteScore: 2)
J. of Cardiothoracic Surgery     Open Access   (Followers: 5, SJR: 0.607, CiteScore: 1)
J. of Cardiovascular Magnetic Resonance     Open Access   (Followers: 1, SJR: 2.292, CiteScore: 5)
J. of Clinical Movement Disorders     Open Access   (Followers: 3)
J. of Congenital Cardiology     Open Access   (Followers: 4)
J. of Cotton Research     Open Access  
J. of Diabetes and Metabolic Disorders     Open Access   (Followers: 8, SJR: 0.818, CiteScore: 2)
J. of Eating Disorders     Open Access   (Followers: 9, SJR: 0.693, CiteScore: 1)
J. of Environmental Health Science & Engineering     Open Access   (Followers: 1, SJR: 0.802, CiteScore: 3)
J. of Ethnobiology and Ethnomedicine     Open Access   (SJR: 0.693, CiteScore: 3)
J. of Experimental & Clinical Cancer Research     Open Access   (Followers: 3, SJR: 2, CiteScore: 6)
J. of Foot and Ankle Research     Open Access   (Followers: 5, SJR: 0.873, CiteScore: 2)
J. of Health, Population and Nutrition     Open Access   (Followers: 9, SJR: 0.875, CiteScore: 2)
J. of Hematology & Oncology     Open Access   (Followers: 3, SJR: 2.292, CiteScore: 6)
J. of Inflammation     Open Access   (Followers: 2, SJR: 1.101, CiteScore: 3)
J. of Intensive Care     Open Access   (Followers: 6, SJR: 1.137, CiteScore: 3)
J. of Medical Case Reports     Open Access   (Followers: 1, SJR: 0.331, CiteScore: 1)
J. of Molecular Psychiatry     Open Access   (Followers: 9, SJR: 0.355, CiteScore: 0)
J. of Nanobiotechnology     Open Access   (Followers: 4, SJR: 1.38, CiteScore: 5)
J. of Negative Results in BioMedicine     Open Access   (SJR: 0.483, CiteScore: 1)
J. of Neurodevelopmental Disorders     Open Access   (SJR: 1.71, CiteScore: 4)
J. of NeuroEngineering and Rehabilitation     Open Access   (Followers: 13, SJR: 1.515, CiteScore: 5)
J. of Neuroinflammation     Open Access   (Followers: 2, SJR: 2.336, CiteScore: 5)
J. of Occupational Medicine and Toxicology     Open Access   (Followers: 13, SJR: 0.591, CiteScore: 2)
J. of Orthopaedic Surgery and Research     Open Access   (Followers: 6, SJR: 0.751, CiteScore: 2)
J. of Otolaryngology - Head and Neck Surgery     Open Access   (Followers: 10, SJR: 0.827, CiteScore: 2)
J. of Ovarian Research     Open Access   (SJR: 1.008, CiteScore: 3)
J. of Pharmaceutical Policy and Practice     Open Access   (Followers: 4, SJR: 0.545, CiteScore: 1)
J. of Physiological Anthropology     Open Access   (Followers: 8, SJR: 0.514, CiteScore: 2)
J. of the Intl. AIDS Society     Open Access   (Followers: 8, SJR: 2.092, CiteScore: 4)
J. of the Intl. Society of Sports Nutrition     Open Access   (Followers: 57, SJR: 0.775, CiteScore: 2)
J. of Therapeutic Ultrasound     Open Access   (SJR: 0.906, CiteScore: 3)
J. of Translational Medicine     Open Access   (Followers: 4, SJR: 1.565, CiteScore: 4)
J. of Trauma Management & Outcomes     Open Access   (Followers: 5, SJR: 0.398, CiteScore: 1)
J. of Venomous Animals and Toxins including Tropical Diseases     Open Access   (Followers: 1, SJR: 0.573, CiteScore: 2)
Kidney Disease and Transplantation     Open Access   (Followers: 4)
Lipids in Health and Disease     Open Access   (SJR: 0.915, CiteScore: 2)
Longevity & Healthspan     Open Access   (Followers: 1)
Malaria J.     Open Access   (Followers: 8, SJR: 2.082, CiteScore: 3)
Marine Biodiversity Records     Open Access   (Followers: 4, SJR: 0.354, CiteScore: 1)
Microbial Cell Factories     Open Access   (Followers: 8, SJR: 1.443, CiteScore: 4)
Military Medical Research     Open Access   (Followers: 2, SJR: 0.601, CiteScore: 2)
Mobile DNA     Open Access   (SJR: 3.783, CiteScore: 5)
Molecular Autism     Open Access   (Followers: 9, SJR: 2.377, CiteScore: 5)
Molecular Brain     Open Access   (Followers: 3, SJR: 1.805, CiteScore: 4)
Molecular Cancer     Open Access   (Followers: 4, SJR: 2.778, CiteScore: 7)
Molecular Cytogenetics     Open Access   (Followers: 1, SJR: 0.623, CiteScore: 1)
Molecular Neurodegeneration     Open Access   (Followers: 2, SJR: 3.418, CiteScore: 7)
Movement Ecology     Open Access   (Followers: 9, SJR: 2.242, CiteScore: 4)
Multidisciplinary Respiratory Medicine     Open Access   (Followers: 3, SJR: 1.13, CiteScore: 2)
Multiple Sclerosis and Demyelinating Disorders     Open Access   (Followers: 5)
Neural Development     Open Access   (Followers: 2, SJR: 1.821, CiteScore: 2)
NeuroMetals     Open Access  
Neuropsychiatric Electrophysiology     Open Access  
Neurovascular Imaging     Open Access  
Nutrition & Metabolism     Open Access   (Followers: 10)
Nutrition J.     Open Access   (Followers: 7, SJR: 1.447, CiteScore: 4)
Orphanet J. of Rare Diseases     Open Access   (Followers: 1, SJR: 1.413, CiteScore: 3)
Particle and Fibre Toxicology     Open Access   (Followers: 2, SJR: 2.253, CiteScore: 8)
Patient Safety in Surgery     Open Access   (Followers: 4, SJR: 0.525, CiteScore: 1)
Pediatric Rheumatology     Open Access   (Followers: 7, SJR: 0.729, CiteScore: 2)
Philosophy, Ethics, and Humanities in Medicine     Open Access   (Followers: 1, SJR: 0.285, CiteScore: 1)
Pilot and Feasibility Studies     Open Access   (Followers: 1)
Plant Methods     Open Access   (Followers: 2, SJR: 1.885, CiteScore: 4)
PMC Biophysics     Open Access  
Population Health Metrics     Open Access   (Followers: 5, SJR: 1.954, CiteScore: 3)
Porcine Health Management     Open Access  
Proteome Science     Open Access   (Followers: 1, SJR: 0.792, CiteScore: 2)
Public Health Reviews     Open Access   (Followers: 2, SJR: 0.454, CiteScore: 1)
Radiation Oncology     Open Access   (Followers: 6, SJR: 1.293, CiteScore: 3)
Renal Replacement Therapy     Open Access   (Followers: 4)
Reproductive Biology and Endocrinology     Open Access   (Followers: 4, SJR: 1.203, CiteScore: 3)
Reproductive Health     Open Access   (Followers: 2, SJR: 1.228, CiteScore: 2)
Research Involvement and Engagement     Open Access  
Respiratory Research     Open Access   (Followers: 1, SJR: 1.644, CiteScore: 4)
Retrovirology     Open Access   (SJR: 1.855, CiteScore: 3)
Safety in Health     Open Access   (Followers: 59)
Scandinavian J. of Trauma, Resuscitation and Emergency Medicine     Open Access   (Followers: 12, SJR: 0.618, CiteScore: 2)
Scoliosis     Open Access   (Followers: 3)
Scoliosis and Spinal Disorders     Open Access   (Followers: 1, SJR: 0.843, CiteScore: 2)
Skeletal Muscle     Open Access   (Followers: 1, SJR: 2.32, CiteScore: 4)
Source Code for Biology and Medicine     Open Access   (SJR: 0.784, CiteScore: 2)
Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology     Open Access   (Followers: 17)
Standards in Genomic Sciences     Open Access   (SJR: 0.768, CiteScore: 2)
Stem Cell Research & Therapy     Open Access   (Followers: 10, SJR: 1.685, CiteScore: 5)
Substance Abuse Treatment, Prevention and Policy     Open Access   (Followers: 8, SJR: 1.108, CiteScore: 2)
Sustainable Earth     Open Access  
Systematic Reviews     Open Access   (Followers: 11, SJR: 1.794, CiteScore: 4)
Theoretical Biology and Medical Modelling     Open Access   (Followers: 1, SJR: 0.783, CiteScore: 2)
Thrombosis J.     Open Access   (Followers: 4, SJR: 1.009, CiteScore: 3)
Thyroid Research     Open Access   (Followers: 1, SJR: 0.329, CiteScore: 1)
Tobacco Induced Diseases     Open Access   (Followers: 9, SJR: 0.716, CiteScore: 2)
Translational Neurodegeneration     Open Access   (Followers: 1, SJR: 1.901, CiteScore: 5)
Trials     Open Access   (Followers: 3, SJR: 1.291, CiteScore: 2)
Tropical Diseases, Travel Medicine and Vaccines     Open Access   (Followers: 1)
Vascular Cell     Open Access   (SJR: 1.349, CiteScore: 4)
Veterinary Research     Open Access   (Followers: 11)
Virology J.     Open Access   (Followers: 7, SJR: 1.053, CiteScore: 2)
Women's Midlife Health     Open Access   (Followers: 1)
World Allergy Organization J.     Open Access   (Followers: 1, SJR: 1.936, CiteScore: 6)
World J. of Emergency Surgery     Open Access   (Followers: 5, SJR: 1.098, CiteScore: 3)
World J. of Surgical Oncology     Open Access   (Followers: 1, SJR: 0.688, CiteScore: 2)

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Journal of Experimental & Clinical Cancer Research
Journal Prestige (SJR): 2
Citation Impact (citeScore): 6
Number of Followers: 3  

  This is an Open Access Journal Open Access journal
ISSN (Print) 0392-9078 - ISSN (Online) 1756-9966
Published by BMC (Biomed Central) Homepage  [310 journals]
  • Immunotherapy of brain metastases: breaking a “dogma”

    • Abstract: Until very few years ago, the oncology community dogmatically excluded any clinical potential for immunotherapy in controlling brain metastases. Therefore, despite the significant therapeutic efficacy of monoclonal antibodies to immune check-point(s) across a wide range of tumor types, patients with brain disease were invariably excluded from clinical trials with these agents. Recent insights on the immune landscape of the central nervous system, as well as of the brain tumor microenvironment, are shedding light on the immune-biology of brain metastases. Interestingly, retrospective analyses, case series, and initial prospective clinical trials have recently investigated the role of different immune check-point inhibitors in brain metastases, reporting a significant clinical activity also in this subset of patients. These findings, and their swift translation in the daily practice, are driving fundamental changes in the clinical management of patients with brain metastases, and raise important neuroradiologic challenges. Along this line, neuro-oncology undoubtedly represents an additional area of active investigation and of growing interest to support medical oncologists in the evaluation of clinical responses of brain metastases to ICI treatment, and in the management of neurologic immune-related adverse events. Aim of this review is to summarize the most recent findings on brain metastases immunobiology, on the evolving scenario of clinical efficacy of ICI therapy in patients with brain metastases, as well as on the increasing relevance of neuroradiology in this therapeutic setting.
      PubDate: 2019-10-17
  • LINC00673 is activated by YY1 and promotes the proliferation of breast
           cancer cells via the miR-515-5p/MARK4/Hippo signaling pathway

    • Abstract: Background An increasing number of studies have shown that long noncoding RNAs (lncRNAs) play essential roles in tumor initiation and progression. LncRNAs act as tumor promoters or suppressors by targeting specific genes via epigenetic modifications and competing endogenous RNA (ceRNA) mechanisms. In this study, we explored the function and detailed mechanisms of long intergenic nonprotein coding RNA 673 (LINC00673) in breast cancer progression. Methods Quantitative real-time PCR (qRT-PCR) was used to examine the expression of LINC00673 in breast cancer tissues and in adjacent normal tissues. Gain-of-function and loss-of function experiments were conducted to investigate the biological functions of LINC00673 in vitro and in vivo. We also explored the potential role of LINC00673 as a therapeutic target using antisense oligonucleotide (ASO) in vivo. RNA sequencing (RNA-seq), dual-luciferase reporter assays, chromatin immunoprecipitation (ChIP) assay, and rescue experiments were performed to uncover the detailed mechanism of LINC00673 in promoting breast cancer progression. Results In the present study, LINC00673 displayed a trend of remarkably increased expression in breast cancer tissues and was associated with poor prognosis in breast cancer patients. Importantly, LINC00673 depletion inhibited breast cancer cell proliferation by inhibiting the cell cycle and increasing apoptosis. Furthermore, ASO therapy targeting LINC00673 substantially suppressed breast cancer cell proliferation in vivo. Mechanistically, LINC00673 was found to act as a ceRNA by sponging miR-515-5p to regulate MARK4 expression, thus inhibiting the Hippo signaling pathway. Finally, ChIP assay showed that the transcription factor Yin Yang 1 (YY1) could bind to the LINC00673 promoter and increase its transcription in cis. Conclusions YY1-activated LINC00673 may exert an oncogenic function by acting as a sponge for miR-515-5p to upregulate the MARK4 and then inhibit Hippo signaling pathway, and may serve as a potential therapeutic target.
      PubDate: 2019-10-17
  • MEIS2C and MEIS2D promote tumor progression via Wnt/β-catenin and
           hippo/YAP signaling in hepatocellular carcinoma

    • Abstract: Background MEIS2 has been identified as one of the key transcription factors in the gene regulatory network in the development and pathogenesis of human cancers. Our study aims to identify the regulatory mechanisms of MEIS2 in hepatocellular carcinoma (HCC), which could be targeted to develop new therapeutic strategies. Methods The variation of MEIS2 levels were assayed in a cohort of HCC patients. The proliferation, clone-formation, migration, and invasion abilities of HCC cells were measured to analyze the effects of MEIS2C and MEIS2D (MEIS2C/D) knockdown with small hairpin RNAs in vitro and in vivo. Chromatin immunoprecipitation (ChIP) was performed to identify MEIS2 binding site. Immunoprecipitation and immunofluorescence assays were employed to detect proteins regulated by MEIS2. Results The expression of MEIS2C/D was increased in the HCC specimens when compared with the adjacent noncancerous liver (ANL) tissues. Moreover, MEIS2C/D expression negatively correlated with the prognosis of HCC patients. On the other hand, knockdown of MEIS2C/D could inhibit proliferation and diminish migration and invasion of hepatoma cells in vitro and in vivo. Mechanistically, MESI2C activated Wnt/β-catenin pathway in cooperation with Parafibromin (CDC73), while MEIS2D suppressed Hippo pathway by promoting YAP nuclear translocation via miR-1307-3p/LATS1 axis. Notably, CDC73 could directly either interact with MEIS2C/β-catenin or MEIS2D/YAP complex, depending on its tyrosine-phosphorylation status. Conclusions Our studies indicate that MEISC/D promote HCC development via Wnt/β-catenin and Hippo/YAP signaling pathways, highlighting the complex molecular network of MEIS2C/D in HCC pathogenesis. These results suggest that MEISC/D may serve as a potential novel therapeutic target for HCC.
      PubDate: 2019-10-17
  • NANOG helps cancer cells escape NK cell attack by downregulating ICAM1
           during tumorigenesis

    • Abstract: Background At the beginning of tumorigenesis, newly born cancer cells must successfully avoid attack by the immune system. Although most abnormal cells are efficiently identified and destroyed by the immune system, particularly by NK cells, the molecular mechanisms by which newly born cancer cells evade NK cell surveillance are not fully understood. Methods NK cell resistance of highly tumorigenic population of human prostate cancer (PCa) cells were confirmed by xenograft in SCID mice with or without NK cell neutralization. The mechanisms by which the tumorigenic PCa cells evaded NK cell attack were investigated by RNAseq, ChIPseq, generation of several transformants and xenograft in SCID mice. Results Here, we show that PCa cells have a strengthened ability to escape NK cell attack due to NANOG, a pluripotent-related transcription factor, mediating the repression of ICAM1, a cell adhesion molecule, during tumorigenesis. Mechanistically, NANOG directly binds to the region upstream of ICAM1. As the binding between NANOG and the upstream ICAM1 region increases, p300 binding to this region is diminished, resulting in decreased ICAM1 expression. High NANOG expression confers PCa cells the ability to resist NK cell attack via the repression of ICAM1. Consistent with these results, low ICAM1 expression is significantly correlated with a high recurrence rate in patients with PCa. Conclusions Our findings indicate that repression of ICAM1 is a critical mechanism by which cancer cells evade attack from NK cells during tumorigenesis. These results suggest a pivotal role of NANOG in establishing a gene expression profile for escaping the immune system.
      PubDate: 2019-10-16
  • Correction to: FAK-ERK activation in cell/matrix adhesion induced by the
           loss of apolipoprotein E stimulates the malignant progression of ovarian

    • Abstract: In the original publication of this manuscript [1], Fig. 5E lower panel was incorrect due to an error in the preparation of these figures for publication. It was noticed that in the lower panel of Fig. 5E, one mouse image of ApoE−/− + PBS group (upper) was a photograph coming from ApoE−/− + BAPN pre-treatment group (lower). The corrected figure appears below. We apologize for any confusion this may have caused.
      PubDate: 2019-10-15
  • Inhibiting PAD2 enhances the anti-tumor effect of docetaxel in
           tamoxifen-resistant breast cancer cells

    • Abstract: Background Tamoxifen resistance presents a huge clinical challenge for breast cancer patients. An understanding of the mechanisms of tamoxifen resistance can guide development of efficient therapies to prevent drug resistance. Methods We first tested whether peptidylarginine deiminase 2 (PAD2) may be involved in tamoxifen-resistance in breast cancer cells. The effect of depleting or inhibiting PAD2 in tamoxifen-resistant MCF-7 (MCF7/TamR) cells was evaluated both in vitro and in vivo. We then investigated the potential of Cl-amidine, a PAD inhibitor, to be used in combination with tamoxifen or docetaxel, and further explored the mechanism of the synergistic and effective drug regimen of PADs inhibitor and docetaxel on tamoxifen-resistant breast cancer cells. Results We report that PAD2 is dramatically upregulated in tamoxifen-resistant breast cancer. Depletion of PAD2 in MCF7/TamR cells facilitated the sensitivity of MCF7/TamR cells to tamoxifen. Moreover, miRNA-125b-5p negatively regulated PAD2 expression in MCF7/TamR cells, therefore overexpression of miR-125b-5p also increased the cell sensitivity to tamoxifen. Furthermore, inhibiting PAD2 with Cl-amidine not only partially restored the sensitivity of MCF7/TamR cells to tamoxifen, but also more efficiently enhanced the efficacy of docetaxel on MCF7/TamR cells with lower doses of Cl-amidine and docetaxel both in vivo and in vivo. We then showed that combination treatment with Cl-amidine and docetaxel enhanced p53 nuclear accumulation, which synergistically induced cell cycle arrest and apoptosis. Meanwhile, p53 activation in the combination treatment also accelerated autophagy processes by synergistically decreasing the activation of Akt/mTOR signaling, thus enhancing the inhibition of proliferation. Conclusion Our results suggest that PAD2 functions as an important new biomarker for tamoxifen-resistant breast cancers and that inhibiting PAD2 combined with docetaxel may offer a new approach to treatment of tamoxifen-resistant breast cancers.
      PubDate: 2019-10-10
  • CyclinD1 inhibits dicer and crucial miRNA expression by chromatin
           modification to promote the progression of intrahepatic cholangiocarcinoma

    • Abstract: Background CyclinD1 is crucial for cell cycling and can regulate the expression of Dicer, a crucial regulator of microRNA maturation. However, little is known on how CyclinD1 regulates Dicer and miRNA expression, and the progression of intrahepatic cholangiocarcinoma (ICC). Methods The expression of CyclinD1 and Dicer in non-tumor cholangiocytes, ICC cells and tissues as well as their association with clinicopathological characteristics and survival were examined. The potential mechanisms by which CyclinD1 regulates Dicer and relative miRNA expression were determined by immunoprecipitation, ChIP sequence, BSP and luciferase reporter assays following induction of CyclinD1 over-expression or silencing and Dicer silencing. The impact of CyclinD1 and/or Dicer silencing on the growth of ICC was tested in vivo. Results Up-regulated CyclinD1 was associated with down-regulated Dicer expression in ICC tissues and poorer overall survival in patients with ICC. CyclinD1 interacted with the nuclear H3K9me3 and SUV39H1 and bound to the Dicer promoter to increase its CpG island methylation in ICC cells. Functionally, CyclinD1 silencing inhibited the malignancy of ICC cells, which were mitigated partially by Dicer silencing in ICC cells. Dicer silencing down-regulated miR-1914-5p and miR-541-5p expression, which targeted and promoted CyclinD1 and CDK6 expression in ICC cells. Conclusions Our findings uncover that CyclinD1 inhibits Dicer expression by chromatin modification to reduce miR-1914-5p/miR-541-5p expression, which positively-feedback enhances CyclinD1 and CDK6 expression and progression of ICC.
      PubDate: 2019-10-07
  • HOXD9 promotes the growth, invasion and metastasis of gastric cancer cells
           by transcriptional activation of RUFY3

    • Abstract: Background The transcription factor HOXD9 is one of the members of the HOX family, which plays an important role in neoplastic processes. However, the role of HOXD9 in the growth and metastasis of gastric cancer (GC) remains to be elucidated. Methods In vitro functional role of HOXD9 and RURY3 in GC cells was determined using the TMA-based immunohistochemistry, western blot, EdU incorporation, gelatin zymography, luciferase, chromatin Immunoprecipitation (ChIP) and cell invasion assays. In vivo tumor growth and metastasis were conducted in nude mice. Results HOXD9 is overexpressed in GC cells and tissues. The high expression of HOXD9 was correlated with poor survival in GC patients. Functionally, HOXD9 expression significantly promoted the proliferation, invasion and migration of GC cells. Mechanically, HOXD9 directly associated with the RUFY3 promoter to increase the transcriptional activity of RUFY3. Inhibition of RUFY3 attenuated the proliferation, migration and invasiveness of HOXD9-overexpressing GC cells in vitro and in vivo. Moreover, both HOXD9 and RUFY3 were highly expressed in cancer cells but not in normal gastric tissues, with their expressions being positively correlated. Conclusions The evidence presented here suggests that the HOXD9-RUFY3 axis promotes the development and progression of human GC.
      PubDate: 2019-09-23
  • Graphene oxide arms oncolytic measles virus for improved effectiveness of
           cancer therapy

    • Abstract: Background Replication-competent oncolytic viruses (OVs) have been proven to be a potent anticancer weapon for clinical therapy. The preexisting neutralizing antibody in patients is a big challenge for oncolytic efficacy of OVs. Graphene oxide sheets (GOS) possess excellent biological compatibility and are easy to decorate for targeted delivery. Methods We generated PEI-GOS-PEG-FA (Polyethyleneimine-Graphene oxide sheets-Polyethylene glycol-Folic acid). After intravenous injection, the distribution of PEI-GOS-PEG-FA in tumor-bearing mice was visualized by the IVIS Lumina XR system. Then, the oncolytic measles virus (MV-Edm) was coated with PEI-GOS-PEG-FA to form a viral-GOS complex (GOS/MV-Edm). The oncolytic effects of GOS/MV-Edm were investigated both in vitro and in vivo. Results GOS/MV-Edm exhibited higher infectivity and enhanced oncolysis. In tumor-bearing mice, GOS/MV-Edm had significantly elevated viral replication within the tumor mass, and achieved an improved antitumor effect. Then, we confirmed that GOS/MV-Edm entered cancer cells via the folate receptor instead of CD46, a natural cognate receptor of MV-Edm. GOS/MV-Edm remained the infectivity in murine cells that lack CD46. Finally, we found that GOS/MV-Edm was effectively protected from neutralization in the presence of antiserum both in vitro and in vivo. In passively antiserum immunized tumor-bearing mice, the survival was remarkably improved with intravenous injection of GOS/MV-Edm. Conclusion Our findings demonstrate that GOS/MV-Edm displays significantly elevated viral replication within the tumor mass, leading to an improved antitumor effect in solid tumor mouse model. Our study provided a novel strategy to arm OVs for more efficient cancer therapy. That may become a promising therapeutic strategy for cancer patients.
      PubDate: 2019-09-18
  • Long non-coding RNA HOTTIP enhances IL-6 expression to potentiate immune
           escape of ovarian cancer cells by upregulating the expression of PD-L1 in

    • Abstract: Background Long non-coding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP), has been demonstrated to be a vital biomarker when evaluating the prognosis of multiple cancers. Nevertheless, the potential function of HOTTIP in ovarian cancer (OC), a prevalent cancer among women worldwide, remains elusive. Hence, the current study aimed to elucidate the functional relevance of HOTTIP in the development of OC. Methods Positive expression of PD-L1 and IL-6 was determined using immunohistochemical staining in the collected OC and normal tissues. The correlation of IL-6 and PD-L1 was analyzed using flow cytometry, Western blot analysis as well as Pearson’s correlation coefficient. The interaction among HOTTIP, c-jun and IL-6 was investigated with the use of RIP, ChIP and dual luciferase reporter gene assays. Finally, the effects of HOTTIP on T cell proliferation and infiltration were identified through gain- and loss-of-function studies in vitro and in vivo. Results HOTTIP, IL-6 and PD-L1 were all highly expressed in OC tissues. A positive correlation was observed between IL-6 and PD-L1 and that between HOTTIP and IL-6 in OC tissues. HOTTIP was noted to promote the expression of IL-6 by binding to c-jun, which resulted in a promoted PD-L1 expression in neutrophils and immune escape while inhibiting T cell proliferation as well as tumor immunotherapy. Conclusion Taken together, our study unveiled that HOTTIP could promote the secretion of IL-6, and consequently up-regulate the expression of PD-L1 in neutrophils, thus inhibiting the activity of T cells and ultimately accelerating immune escape of OC cells. Our study provides a potential therapeutic strategy by targeting HOTTIP in OC.
      PubDate: 2019-09-18
  • Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of
           hepatocellular carcinoma via interacting with ACTN4

    • Abstract: Background ATPase associated with a variety of cellular activities (AAA ATPase) family members are closely linked to tumor formation and progression. However, their roles in hepatocellular carcinoma (HCC) largely remain unclear. Methods Bioinformatic analyses of public databases were used to excavate the potential AAA ATPases that may contribute to HCC, and thyroid hormone receptor interactor 13 (TRIP13) was selected to following researches because of its most prominently differential expression. Western blot, qRT-PCR and immunohistochemistry were used to detect the expression of TRIP13 in HCC tissues, and then the relationship between TRIP13 expression and clinicopathological parameters were evaluated. Finally, its functions and potential mechanisms were investigated through a series gain- and loss-of-function strategies both in vitro and in vivo. Results TRIP13 was significantly overexpressed in HCC tissues and high level of TRIP13 was closely correlated with a worse clinical outcome. Functionally, elevated TRIP13 facilitated cell proliferation, migration, invasion, and promoted cellular epithelial–mesenchymal transition (EMT) in vitro, while promote tumor growth and lung metastasis in vivo. Mechanistically, TRIP13 interacted with ACTN4 and positively regulated its expression, thus activating the AKT/mTOR pathway to drive tumor progression. Moreover, miR-192-5p served as an upstream regulator of TRIP13 by directly binding to TRIP13 mRNA 3′ UTR, which may partially explain the high expression of TRIP13 in HCC. Conclusion Our findings identified TRIP13 as a promising candidate oncogene in HCC, and TRIP13 induced cell migration, invasion and metastasis of HCC through the AKT/mTOR signaling via interacting with ACTN4.
      PubDate: 2019-09-18
  • UFM1 suppresses invasive activities of gastric cancer cells by attenuating
           the expres7sion of PDK1 through PI3K/AKT signaling

    • Abstract: Background UFM1 has been found to be involved in the regulation of tumor development. This study aims to clarify the role and potential molecular mechanisms of UFM1 in the invasion and metastasis of gastric cancer. Methods Expression of UFM1 in gastric tumor and paired adjacent noncancerous tissues from 437 patients was analyzed by Western blotting, immunohistochemistry, and realtime PCR. Its correlation with the clinicopathological characteristics and prognosis of gastric cancer patients was analyzed. The effects of UFM1 on the invasion and migration of gastric cancer cells were determined by the wound and trans-well assays, and the effect of UFM1 on subcutaneous tumor formation was verified in nude mice. The potential downstream targets of UFM1 and related molecular mechanisms were clarified by the human protein kinase assay and co-immunoprecipitation technique. Results Compared with the corresponding adjacent tissues, the transcription level and protein expression level of UFM1 in gastric cancer tissues were significantly downregulated (P < 0.05). The 5-year survival rate of gastric cancer patients with low UFM1 expression was significantly lower than the patients with high UFM1 expression (42.1% vs 63.0%, P < 0.05). The invasion and migration abilities of gastric cancer cells with stable UFM1 overexpression were significantly decreased, and the gastric cancer cells with UFM1 stable knockdown showed the opposite results; similar results were also obtained in the nude mouse model. Further studies have revealed that UFM1 could increase the ubiquitination level of PDK1 and decrease the expression of PDK1 at protein level, thereby inhibiting the phosphorylation level of AKT at Ser473. Additionally, the effect of UFM1 on gastric cancer cell function is dependent on the expression of PDK1. The expression level of UFM1 can improve the poor prognosis of PDK1 in patients with gastric cancer. Conclusion UFM1 suppresses the invasion and metastasis of gastric cancer by increasing the ubiquitination of PDK1 through negatively regulating PI3K/AKT signaling.
      PubDate: 2019-09-18
  • Correction to: Synergistic killing effects of homoharringtonine and
           arsenic trioxide on acute myeloid leukemia stem cells and the underlying

    • Abstract: In the publication of this article [1], there are two corrections.
      PubDate: 2019-09-16
  • SCP2-mediated cholesterol membrane trafficking promotes the growth of
           pituitary adenomas via Hedgehog signaling activation

    • Abstract: Background Metabolic reprogramming is an important characteristic of tumors. In the progression of pituitary adenomas (PA), abnormal glucose metabolism has been confirmed by us before. However, whether cholesterol metabolism is involved in the process of PA remains unclear. This study aimed to investigate whether abnormal cholesterol metabolism could affect the progression of PA. Methods We analyzed the expression of sterol carrier protein 2 (SCP2) in 40 surgical PA samples. In vitro experiments and xenograft models were used to assess the effects of SCP2 and cholesterol on proliferation of PA. The incidence of hypercholesterolemia between 140 PA patients and 100 heathy controls were compared. Results We found an upregulation of SCP2 in PA samples, especially in tumors with high proliferation index. Forced expression of SCP2 promoted PA cell lines proliferation in vitro. Furthermore, SCP2 regulated cholesterol trafficking from cytoplasm to membrane in GH3 cells, and extracellularly treating GH3 cells and primary PA cells with methyl-β-cyclodextrin/cholesterol complex to mimic membrane cholesterol concentration enhanced cell proliferation, which suggested a proliferative effect of cholesterol. Mechanistically, cholesterol induced activation of PKA/SUFU/GLI1 signaling via smoothened receptor, which was well-known as Hedgehog signaling, resulting in inhibiting apoptosis and promoting cell cycle. Accordingly, activation of Hedgehog signaling was also confirmed in primary PA cells and surgical PA samples. In vivo, SCP2 overexpression and high cholesterol diet could promote tumor growth. Intriguingly, the incidence of hypercholesterolemia was significantly higher in PA patients than healthy controls. Conclusions Our data indicated that dysregulated cholesterol metabolism could promote PA growth by activating Hedgehog signaling, supporting a potential tumorigenic role of cholesterol metabolism in PA progression.
      PubDate: 2019-09-13
  • Iron and leukemia: new insights for future treatments

    • Abstract: Iron, an indispensable element for life, is involved in all kinds of important physiological activities. Iron promotes cell growth and proliferation, but it also causes oxidative stress damage. The body has a strict regulation mechanism of iron metabolism due to its potential toxicity. As a cancer of the bone marrow and blood cells, leukemia threatens human health seriously. Current studies suggest that dysregulation of iron metabolism and subsequent accumulation of excess iron are closely associated with the occurrence and progress of leukemia. Specifically, excess iron promotes the development of leukemia due to the pro-oxidative nature of iron and its damaging effects on DNA. On the other hand, leukemia cells acquire large amounts of iron to maintain rapid growth and proliferation. Therefore, targeting iron metabolism may provide new insights for approaches to the treatment of leukemia. This review summarizes physiologic iron metabolism, alternations of iron metabolism in leukemia and therapeutic opportunities of targeting the altered iron metabolism in leukemia, with a focus on acute leukemia.
      PubDate: 2019-09-13
  • Dihydroartemisinin-induced unfolded protein response feedback attenuates
           ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells

    • Abstract: Background Dihydroartemisinin (DHA) has been shown to exert anticancer activity through iron-dependent reactive oxygen species (ROS) generation, which is similar to ferroptosis, a novel form of cell death. However, whether DHA causes ferroptosis in glioma cells and the potential regulatory mechanisms remain unclear. Methods Effects of DHA on the proliferation, cell death, ROS and lipid ROS generation as well as reduced gluthione consumption were assessed in glioma cells with or without ferroptosis inhibitor. The biological mechanisms by which glioma cells attenuate the pro-ferroptotic effects of DHA were assessed using molecular methods. Results DHA induced ferroptosis in glioma cells, as characterized by iron-dependent cell death accompanied with ROS generation and lipid peroxidation. However, DHA treatment simultaneously activated a feedback pathway of ferroptosis by increasing the expression of heat shock protein family A (Hsp70) member 5 (HSPA5). Mechanistically, DHA caused endoplasmic reticulum (ER) stress in glioma cells, which resulted in the induction of HSPA5 expression by protein kinase R-like ER kinase (PERK)-upregulated activating transcription factor 4 (ATF4). Subsequent HSPA5 upregulation increased the expression and activity of glutathione peroxidase 4 (GPX4), which neutralized DHA-induced lipid peroxidation and thus protected glioma cells from ferroptosis. Inhibition of the PERK-ATF4-HSPA5-GPX4 pathway using siRNA or small molecules increased DHA sensitivity of glioma cells by increasing ferroptosis both in vitro and in vivo. Conclusions Collectively, these data suggested that ferroptosis might be a novel anticancer mechanism of DHA in glioma and HSPA5 may serve as a negative regulator of DHA-induced ferroptosis. Therefore, inhibiting the negative feedback pathway would be a promising therapeutic strategy to strengthen the anti-glioma activity of DHA.
      PubDate: 2019-09-13
  • Zebrafish modeling reveals that SPINT1 regulates the aggressiveness of
           skin cutaneous melanoma and its crosstalk with tumor immune

    • Abstract: Background Skin cutaneous melanoma (SKCM) is the most lethal form of skin cancer and while incidence rates are declining for most cancers, they have been steadily rising for SKCM. Serine protease inhibitor, kunitz-type, 1 (SPINT1) is a type II transmembrane serine protease inhibitor that has been shown to be involved in the development of several types of cancer, such as squamous cell carcinoma and colorectal cancer. Methods We used the unique advantages of the zebrafish to model the impact of Spint1a deficiency in early transformation, progression and metastatic invasion of SKCM together with in silico analysis of the occurrence and relevance of SPINT1 genetic alterations of the SKCM TCGA cohort. Results We report here a high prevalence of SPINT1 genetic alterations in SKCM patients and their association with altered tumor immune microenvironment and poor patient survival. The zebrafish model reveals that Spint1a deficiency facilitates oncogenic transformation, regulates the tumor immune microenvironment crosstalk, accelerates the onset of SKCM and promotes metastatic invasion. Notably, Spint1a deficiency is required at both cell autonomous and non-autonomous levels to enhance invasiveness of SKCM. Conclusions These results reveal a novel therapeutic target for SKCM.
      PubDate: 2019-09-13
  • Targeting T cell metabolism in the tumor microenvironment: an anti-cancer
           therapeutic strategy

    • Abstract: T cells play important roles in anti-tumor immunity. Emerging evidence has revealed that distinct metabolic changes impact the activation and differentiation of T cells. Tailoring immune responses by manipulating cellular metabolic pathways and the identification of new targets may provide new options for cancer immunotherapy. In this review, we focus on recent advances in the metabolic reprogramming of different subtypes of T cells and T cell functions. We summarize how metabolic pathways accurately regulate T cell development, differentiation, and function in the tumor microenvironment. Because of the similar metabolism in activated T cells and tumor cells, we also describe the effect of the tumor microenvironment on T cell metabolism reprogramming, which may provide strategies for maximal anti-cancer effects and enhancing the immunity of T cells. Thus, studies of T lymphocyte metabolism can not only facilitate the basic research of immune metabolism, but also provide potential targets for drug development and new strategies for clinical treatment of cancer.
      PubDate: 2019-09-13
  • ACLY facilitates colon cancer cell metastasis by CTNNB1

    • Abstract: Background Colon cancer is the second leading cancer worldwide. Recurrent disease and chemotherapeutic drug resistance are very common in the advanced stage of colon cancer. ATP-citrate lyase (ACLY), the first-step rate-controlling enzyme in lipid synthesis, is elevated in colon cancer. However, it remains unclear about the exact role of ACLY in the development of colon cancer metastasis. Methods To evaluate the role of ACLY in colon cancer metastasis, we performed cell migration and invasion assays in two ACLY-deficient colon cancer cell lines. Colon cancer mouse model is used to examine ACLY’s effects on colon metastasis potentials in vivo. We analyzed the correlation between ACLY and CTNNB1 protein in 78 colon cancer patients by Pearson correlation. To finally explore the relationship of ACLY and CTNNB1, we used western blots, migration and invasion assays to confirm that ACLY may regulate metastasis by CTNNB1. Results Our data showed that the abilities of cell migration and invasion were attenuated in ACLY-deficient HCT116 and RKO cell lines. Furthermore, we describe the mechanism of ACLY in promoting colon cancer metastasis in vitro and in vivo. ACLY could stabilize CTNNB1 (beta-catenin 1) protein by interacting, and the complex might promote CTNNB1 translocation through cytoplasm to nucleus, subsequently promote the CTNNB1 transcriptional activity and migration and invasion abilities of colon cancer cells. Immunohistochemical analysis of 78 colon cancer patients showed that the high expression levels of ACLY and CTNNB1 protein was positively correlated with metastasis of colon cancer. Conclusions These results shed new light on the molecular mechanism underlying colon cancer metastasis, which might help in improving therapeutic efficacy.
      PubDate: 2019-09-12
  • FUBP1 promotes neuroblastoma proliferation via enhancing glycolysis-a new
           possible marker of malignancy for neuroblastoma

    • Abstract: Background Neuroblastoma (NB) is one of the deadliest paediatric solid tumours due to its rapid proliferative characteristics. Amplified copies of MYCN are considered the most important marker for the prediction of tumour relapse and progression in NB, but they were only detected in 20–30% of NB patients, indicating there might be other oncogenes in the development of NB. The far upstream element binding protein 1 (FUBP1) was first identified as a transcriptional regulator of the proto-oncogene MYC. However, the expression and role of FUBP1 in NB have not been documented. Methods FUBP1 expression was analysed from GEO database and verified by immunohistochemistry (IHC) and western blotting (WB) in NB tissues and cell lines. Cell proliferation and apoptosis were detected by Cell Counting Kit-8, Colony formation assay, EDU, TUNEL staining and flow cytometric analysis. Several glycolytic metabolites production was confirmed by ELISA and oxygen consuming rate (OCR). Luciferase assay, WB, chromatin immunoprecipitation (CHIP) were used to explore the mechanisms of the effect of FUBP1 on NB. Results FUBP1 mRNA levels were increased along with the increase in International Neuroblastoma Staging System (INSS) stages. High expression of FUBP1 with low N-Myc expression accounted for 44.6% of NB patient samples (n = 65). In addition, FUBP1 protein levels were remarkably increased with NB malignancy in the NB tissue microarray (NB: n = 65; ganglioneuroblastoma: n = 31; ganglioneuroma: n = 27). Furthermore, FUBP1 expression was negatively correlated with patient survival rate but positively correlated with ki67 content. In vitro experiments showed that FUBP1 promotes NB cell proliferation and inhibits cell apoptosis via enhancing glycolysis and ATP production. Mechanistically, FUBP1 inhibited the degradation of HIF1α via downregulation of Von Hippel-Lindau (VHL), the E3 ligase for HIF1α, resulting in upregulation of lactate dehydrogenase isoform B (LDHB) expression to enhance glycolysis. Overexpressed or silenced N-Myc could not regulate FUBP1 or LDHB levels. Conclusions Taken together, our findings demonstrate for the first time that elevated FUBP1 promotes NB glycolysis and growth by targeting HIF1α rather than N-Myc, suggesting that FUBP1 is a novel and powerful oncogene in the development of NB independent of N-Myc and may have potential in the diagnosis and treatment of NB.
      PubDate: 2019-09-11
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
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Fax: +00 44 (0)131 4513327
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