miR-126通过靶向调控Crk基因抑制非小细胞肺癌细胞增殖及侵袭

miR-126 inhibits the proliferation and invasion of non-small cell lung cancer cells by targeting the Crk gene

目的:探究miR-126通过靶向调控Crk基因来调控非小细胞肺癌(NSCLC)细胞增殖及侵袭。方法:应用实时定量PCR检测NSCLC组织及其癌旁肺组织中miR-126和Crk mRNA的表达。应用荧光素酶报告基因系统验证Crk是miR-126的靶基因。在NSCLC细胞转染miR-126 mimics或特异沉默Crk的siRNA后,用MTT法检测NSCLC细胞增殖能力,Transwell测定NSCLC细胞侵袭能力。结果:与癌旁肺组织相比,miR-126在肺癌组织中表达显著降低(P<0.05),Crk mRNA在肺癌组织中表达明显升高(P<0.05)。miR-126直接作用于Crk-3'UTR的预计靶位点;MTT细胞增殖实验及Transwell侵袭实验表明,miR-126过表达或Crk基因沉默均能减弱肺癌细胞增殖及侵袭能力(P<0.05)。结论:miR-126通过靶向调控Crk来抑制NSCLC细胞的增殖及侵袭。

Objective:To investigate how miR-126 regulates the proliferation and invasiveness of NSCLC cells by targeting the Crk gene.Methods:Real-time quantitative PCR was used to detect the expressions of miR-126 and Crk mRNA in NSCLC tissues and adjacent lung tissues.The luciferase reporter gene system was used to verify that Crk was the target gene of miR-126.After NSCLC cells were transfected with miR-126 mimics or specific silenced Crk siRNA,the proliferation of NSCLC cells was detected by MTT assay,and the invasiveness of NSCLC cells was determined by Transwell.Results:Compared with adjacent tissues,miR-126 expression was significantly reduced in cancer tissues(P<0.05),and Crk mRNA expression was significantly increased in lung cancer tissues(P<0.05).miR-126 directly acted on the predicted target sites of Crk-3'UTR.MTT cell proliferation test and Transwell invasion test showed that miR-126 overexpression or Crk gene silencing could reduce the proliferation and invasion ability of lung cancer cells(P<0.05).Conclusion:miR-126 inhibits the proliferation and invasion of NSCLC cells by targeting Crk.