microRNA-613调控CDK14来抑制老年胶质瘤患者瘤细胞的增殖和侵袭作用

目的 探讨microRNA-613调控细胞周期蛋白依赖性激酶14(CDK14)通路来抑制老年胶质瘤患者瘤细胞增殖和侵袭的机制。方法 购自上海北诺生物科技有限公司的人脑胶质瘤细胞株U251共24株,分为shNC组、shmicroRNA-613组、Vector组、microRNA-613组,每组各6株; Western Blotting法和qRT-PCR法检测敲减microRNA-613和过表达microRNA-613后的人脑胶质瘤细胞株U251中CDK14蛋白表达水平,CCK-8细胞增殖实验、Transwell小室实验验证敲除microRNA-613和过表达microRNA-613后U251细胞的增殖、侵袭能力。结果 人胶质瘤细胞株U251敲减microRNA-613后CDK14蛋白表达增加(P<0.05); 人胶质瘤细胞株U251过表达microRNA-613后CDK14蛋白表达减少(P<0.05); 转染第24、36、48 h microRNA-613组U251细胞增殖率P<0.05); microRNA-613组U251细胞侵袭能力>Vector组,shNC组>shmicroRNA-613组(P<0.05)。结论 microRNA-613可通过调控CDK14信号转导通路来抑制人脑胶质瘤细胞U251增殖、转移。

Inhibitory effect of Microrna-613 on the proliferation and invasion of cancer cells in ederly glioma patients by regulating CDK14

ObjectiveTo investigate the mechanism of inhibitory effect of microRNA-613 on the proliferation and invasion of cancer cells in elderly glioma patients by regulating cyclin-dependent kinase 14(CDK14).Methods A total of 24 human glioma cell lines U251 purchased from Shanghai Beinuo Biology Co Ltd were divided into shNC group, shmicroRNA-613 group, Vector group, and microRNA-613 group, each with 6 strains. The CDK14 protein expression level, proliferation and invasion ability of U251 cells with knocked-down microRNA-613 and over-expressedmicroRNA-613 were detected by Western Blotting, qRT-PCR, CCK-8 and Transwell chamber assay.Results The CDK14 protein expression level in U251 cells increased after knocking down microRNA-613(P<0.05), and decreased after over-expressingmicroRNA-613(P<0.05). At 24^th, 36 ^th, and 48 ^th h after transfection, the proliferation rate of U251 cells was the lowest in microRNA-613 group, followed by Vector group, shNC group, and shmicroRNA-613 group(P<0.05), meanwhile, the invasion ability of U251 cells was the highest in microRNA-613 group, followed by Vector group, shNC group, and shmicroRNA-613 group(P<0.05).Conclusion MicroRNA-613 could inhibit the proliferation and metastasis of human glioma cells U251 by regulating the CDK14 signal pathway.