miR-150-5p调控非小细胞肺癌的A549细胞凋亡的机制研究  

Mechanism of miR-150-5p in Regulating the Apoptosis of A549 Cells in Non-small Cell Lung Cancer

作　　者：董延琥[1] 王艺静 DONG Yanhu;WANG Yijing(Puyang People's Hospital,Puyang,457000)

机构地区：[1]河南省濮阳市人民医院,457000

出　　处：《实用癌症杂志》2021年第8期1219-1223,共5页The Practical Journal of Cancer

基　　金：河南省自然科学基金项目(编号:182300410342)。

摘　　要：目的探讨miR-150-5p调控非小细胞肺癌A549细胞凋亡的分子机制。方法过表达或敲低miR-150-5p后,检测非小细胞肺癌A549的凋亡水平。敲低miR-150-5p后,检测miRDB数据库在线分析的靶标的mRNA水平。通过荧光素酶报告系统检测miRNA是否与潜在靶标直接结合。过表达或敲低靶标后,分析非小细胞肺癌A549的凋亡水平。结果过表达miR-150-5p后,非小细胞肺癌A549细胞的凋亡水平显著下降(P<0.05);敲低miR-150-5p后,非小细胞肺癌A549细胞的凋亡水平显著上升(P<0.05)。过表达miR-150-5p后,非小细胞肺癌A549细胞中PDIA6和TADA1的表达显著下降(P<0.05);敲低miR-150-5p后,非小细胞肺癌A549细胞中PDIA6和TADA1的表达显著上升(P<0.05)。敲低PDIA6的非小细胞肺癌A549细胞的凋亡水平明显下降(P<0.05),而敲低TADA1的非小细胞肺癌A549细胞的凋亡水平无显著变化(P>0.05)。miR-150-5p靶向PDIA6(P<0.05)。过表达PDIA6后,非小细胞肺癌A549细胞的凋亡水平明显上升(P<0.05)。同时敲低miR-150-5p和PDIA6后,发现非小细胞肺癌A549细胞的凋亡水平无显著变化(P>0.05);同时过表达miR-150-5p和PDIA6后,发现非小细胞肺癌A549细胞的凋亡水平无显著变化(P>0.05)。结论miR-150-5p靶向PDIA6的mRNA,抑制了PDIA6的表达后可降低了非小细胞肺癌A549细胞的凋亡水平。Objective To investigate the molecular mechanism of miR-150-5 p regulating the apoptosis of non-small cell lung cancer A549 cells.Methods After overexpression or knockdown of miR-150-5 p,the apoptosis level of non-small cell lung cancer A549 was detected.After miR-150-5 p was knocked down,the mRNA levels of the targets analyzed online by the miRDB database were detected.The luciferase reporter system was used to detect whether miRNAs were directly bound to potential targets.After overexpression or knockdown of the target,the apoptosis level of non-small cell lung cancer A549 was analyzed.ResultsAfter miR-150-5 p overexpression,the apoptosis level of non-small cell lung cancer A549 cells decreased significantly(P<0.05);after miR-150-5 p was knocked down,the apoptosis level of non-small cell lung cancer A549 cells increased significantly.(P<0.05).After overexpression of miR-150-5 p,the expression of PDIA6 and TADA1 in non-small cell lung cancer A549 cells decreased significantly(P<0.05);after miR-150-5 p was knocked down,the expression of PDIA6 and TADA1 in non-small cell lung cancer A549 cells Significantly increased(P<0.05).Apoptosis level of non-small cell lung cancer A549 cells that knocked down PDIA6 significantly decreased(P<0.05),but there was no significant change in the apoptosis level of non-small cell lung cancer A549 cells that knocked down TADA1(P>0.05).miR-150-5 p targets PDIA6(P<0.05).After overexpression of PDIA6,the apoptosis level of non-small cell lung cancer A549 cells increased significantly(P<0.05).After miR-150-5 p and PDIA6 were knocked down at the same time,there was no significant change in the apoptosis level of non-small cell lung cancer A549 cells(P>0.05);after overexpression of miR-150-5 p and PDIA6,non-small cell lung cancer A549 was found There was no significant change in the apoptosis level of the cells(P>0.05).Conclusion miR-150-5 p targets the mRNA of PDIA6,inhibits the expression of PDIA6,and reduces the apoptosis of non-small cell lung cancer A549 cells.

关 键 词：miR-150-5p PDIA6 非小细胞肺癌 A549细胞 凋亡 

分 类 号：R734.2[医药卫生—肿瘤]