MicroRNA-490-5p靶向CDK1通过ERK信号通路参与胃癌细胞周期调控

作者:侯东泽;代劲松;邓志波;颜登高; 刊名:现代肿瘤医学 上传者:童雷

【摘要】目的:探讨miR-490-5p对胃癌细胞增殖与周期的调控作用和分子机制,以期为临床治疗胃癌提供新的有效靶点。方法:收集30例胃癌患者的胃癌组织及相应的癌旁组织标本;采用Real-time PCR法检测miR-490-5p和CDK1的表达水平;分析细胞周期相关蛋白CDK1与miR-490-5p的靶向关系。MTT法和流式细胞仪检测转染后胃癌细胞生长以及细胞周期情况。结果:与癌旁组织相比,胃癌组织中miR-490-5p的表达显著下调(P<0.001);转染miR-490-5p mimics的细胞中miR-490-5p的表达显著上调,而miR-490-5p inhibitors中miR-490-5p显著下降(均P<0.001);CDK1是miR-490-5p的靶基因;下调miR-490-5p、上调CDK1能促进胃癌细胞的增殖能力及G1/S期的转化(均P<0.001)。结论:通过上调miR-490-5p可以抑制胃癌细胞的恶性增殖,减少CDK1表达,抑制ERK信号途径,降低了G1/S期的转化速率,从而为胃癌诊断及治疗提供新靶标。

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MicroRNA - 490 - 5p 靶向 CDK1 通过 ERK 信号通路参与胃癌细胞周期调控 侯东泽,代劲松,邓志波,颜登高 Overexpression of microRNA-490 -5p targeting CDK1 suppresses proliferation and cell cycle progression of gastric cancer cells by inhibiting ERK signaling pathway Hou Dongze,Dai Jingsong,Deng Zhibo,Yan Denggao Department of General Surgery,Jianli People's Hospital,Hubei Jianli 433300,China. 【Abstract】 Objective: To investigate the effects of microRNA -490 -5p( miR -490 -5p) on the cell proliferation and cell cycle progression in gastric cancer( GC) . Methods: Thirty GC tissues and relative adjacent normal tissues were collected. Quantitative real - time polymerase chain reaction( qRT - PCR) was performed to detect the expression of miR -490 -5p and cyclin dependent kinases( CDK) . The target relationship of miR -490 -5p and CDK1 was an-alyzed. Cell growth and cell cycle were detected using MTT assay and flow cytometry,respectively. Results: miR -490 -5p was significantly down - regulated in GC tissues compared to that in the adjacent normal tissues( P < 0. 001) .miR -490 -5p was highly expressed in the cells transfected with miR -490 -5p mimics but significantly down - reg-ulated in those transfected with the miR -490 -5p inhibitors( both P <0. 001) . miR -490 -5p targeted CDK1. Down - regulating miR -490 -5p and up - regulating CDK1 expression promoted the proliferation and G1 /S transition of GC cells by targeting CDK1( all P < 0. 001) . Conclusion: The proliferation of GC cells could be inhibited by up -regul

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