摘要
目的探讨MiR-23a靶向HOXC8在肾癌发生中的作用及机制。方法选取2019年1月培养的大鼠60例,MiR-23a inhibitor转染组(实验组)20例,空载体转染组20例(阴性对照组),空白组20例(空白对照组)。所有大鼠均进行体内与体外两种实验方法。实施方法主要包括细胞培养、细胞转染、反转录反应、引物扩增、实时定量聚合酶链式反应(polymerase chain reaction,PCR)实验方法、蛋白质免疫印迹(Western Blot实验)、动物实验等。结果在三组肾癌细胞系中转染MiR-23a inhibator后抑制的细胞增殖,促进了细胞凋亡,降低了细胞侵袭性,同时HOXC8的表达也下调,MiR-23a inhibitor转染组HK-2、786-O、CAKI-1、HOXC8均显著低于空载体转染组及空白组,组间比较差异有统计学意义(P<0.05)。在体内实验中转染MiR-23a inhibitor后抑制了肿瘤的生长,其机制与下调HOXC8的表达有关。结论本研究结果提示MiR-23a是肾癌发生发展过程中的一个癌基因,MiR-23a靶向HOXC8的相关性来看,可能是肾癌的一个新的治疗靶点。
Objective To investigate the role and mechanism of MiR-23a targeting HOXC8 in renal cell carcinoma.Methods 60 rats cultured in January 2019 were selected,including 20 cases of MiR-23a inhibitor transfection group(experimental group),20 cases of empty vector transfection group(negative control group),and 20 cases of blank group(blank control group).All rats were tested in vivo and in vitro.The implementation methods include cell culture,cell transfection,reverse transcription reaction,primer amplification,real-time quantitative PCR,Western blot and animal experiment.Results MiR-23a inhibator inhibited cell proliferation,promoted cell apoptosis,reduced cell invasion,and down regulated the expression of HOXC8.The levels of HK-2,786-O,CAKI-1 and HOXC8 in MiR-23a inhibitor transfection group were significantly lower than those in empty vector transfection group and blank group,there were significant differences between the two groups(P<0.05).In vivo,transfection of MiR-23a inhibitor inhibited the growth of tumor,which was related to the down regulation of HOXC8 expression.Conclusion Our results suggest that MiR-23a is a oncogene in the development of renal cell carcinoma,and MiR-23a may be a new therapeutic target for renal cell carcinoma.
作者
张锐
ZHANG Rui(Department of Urology,Heilongjiang Provincial Hospital,Harbin Heilongjiang 150036,China)
出处
《中国卫生标准管理》
2021年第16期125-127,共3页
China Health Standard Management
基金
黑龙江省卫生健康委科研课题(名称:MiR-23a靶向HOXC8在肾癌发生中的作用及机制,编号:2019-153)。
