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MicroRNA‐520c enhances cell proliferation, migration, and invasion by suppressing IRF2 in gastric cancer

机译:MicroRNA-520c通过抑制胃癌中的IRF2增强细胞增殖,迁移和侵袭

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Dysregulation of microRNA (miRNA) is actively involved in the development and progression of gastric cancer (GC). MiR‐520c was previously found to be overexpressed in GC specimens and cells. However, the clinical significance of miR‐520c and its biological function in GC remain largely unknown. Here, we found that miR‐520c expression in GC tissues was significantly increased compared to normal adjacent gastric tissues. Its increased level was prominently correlated with poor clinical parameters and prognosis of GC patients. Accordingly, the expression of miR‐520c was obviously elevated in GC cell lines as compared with gastric epithelial cells. Overexpression of miR‐520c in N‐87 cells significantly increased the proliferative ability, migration, and invasion of cancer cells, while miR‐520c silencing suppressed MKN‐45 cell proliferation, migration, and invasion in vitro. Mechanically, miR‐520c inversely regulated interferon regulatory factor 2 (IRF2) abundance in GC cells. Herein, IRF2 was found to be a downstream target of miR‐520c in GC. Furthermore, IRF2 was down‐regulated in GC tissues compared to nontumor tissues. An inverse correlation between IRF2 and miR‐520c expression was observed in GC cases. Taken together, miR‐520c may serve as a prognostic predictor and a therapeutic target for GC patients.
机译:microRNA(miRNA)的失调积极参与胃癌(GC)的发展和进程。以前发现MiR-520c在GC标本和细胞中过表达。但是,miR-520c的临床意义及其在GC中的生物学功能仍然未知。在这里,我们发现与正常的邻近胃组织相比,GC组织中的miR-520c表达显着增加。其升高的水平与不良的临床参数和GC患者的预后显着相关。因此,与胃上皮细胞相比,miR-520c在GC细胞系中的表达明显升高。 miR-520c在N-87细胞中的过表达显着增加了癌细胞的增殖能力,迁移和侵袭,而miR-520c沉默在体外抑制了MKN-45细胞的增殖,迁移和侵袭。机械上,miR-520c对GC细胞中干扰素调节因子2(IRF2)的丰度具有反向调节作用。在本文中,发现IRF2是GC中miR-520c的下游靶标。此外,与非肿瘤组织相比,GC组织中的IRF2被下调。在GC病例中观察到IRF2和miR-520c表达呈负相关。两者合计,miR-520c可以作为GC患者的预后指标和治疗目标。

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