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首页> 外文期刊>Oncology Research >miR-365 Suppresses Cholangiocarcinoma Cell Proliferation and Induces Apoptosis by Targeting E2F2
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miR-365 Suppresses Cholangiocarcinoma Cell Proliferation and Induces Apoptosis by Targeting E2F2

机译:miR-365抑制胆管癌细胞增殖并通过靶向E2F2诱导细胞凋亡

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Cholangiocarcinoma (CCA) is one of the most malignant adenocarcinomas arising from bile duct epithelial cells. However, the molecular mechanism regulating CCA development and progression still needs to be investigated. Here we found that miR-365 was downregulated in CCA tissues compared with adjacent normal tissues. By functional experiments, we found that overexpression of miR-365 significantly inhibited CCA cell proliferation and promoted cellular apoptosis in vitro. Furthermore, administration with miR-365 markedly suppressed the growth of tumor tissues in vivo. Mechanistically, we identified E2F2 as the target gene of miR365 in CCA cells. We found that overexpression significantly inhibited the expression of E2F2 in CCA cells, and there was an inverse correlation between the expression levels of E2F2 and miR-365 in CCA tissues. We also found that E2F2 was highly expressed in CCA tissues and cell lines. Restoration of E2F2 in miR-365overexpressing CCA cells promoted cell viability and reduced cellular apoptosis in CCA. Collectively, our study demonstrated the essential role of miR-365 and its functional mechanism in CCA cells, which provided a new insight on the design of therapeutic targets for CCA treatment.
机译:胆管癌(CCA)是胆管上皮细胞产生的最恶性肿瘤腺癌之一。但是,调节CCA开发和进展的分子机制仍然需要调查。在这里,我们发现与相邻的正常组织相比,在CCA组织中下调miR-365。通过功能实验,我们发现MiR-365的过度表达显着抑制CCA细胞增殖和促进体外细胞凋亡。此外,用miR-365给药显着抑制了体内肿瘤组织的生长。机械地,我们将E2F2鉴定为CCA细胞中miR365的靶基因。我们发现过表达显着抑制了CCA细胞中E2F2的表达,并且CCA组织中E2F2和miR-365的表达水平之间存在反比相关性。我们还发现E2F2在CCA组织和细胞系中高表达。恢复MiR-365大规处CCA细胞中的E2F2促进细胞活力并降低CCA细胞凋亡。集体,我们的研究表明MIR-365的基本作用及其在CCA细胞中的功能机制,为CCA治疗的治疗靶标设计提供了新的洞察。

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