长链非编码RNA MALAT-1通过EZH2-β-catenin信号通路调控肾癌细胞的增殖、凋亡及侵袭  

Long-chain non-coding RNA MALAT-1 inhibits proliferation and invasion and induces apoptosis of renal cell carcinoma cells by regulating EZH2-β-catenin signaling pathway

作　　者：彭浩[1] 武玉东[2] 李健[1] 李浩[1] 刘愿光 PENG Hao;WU Yu-dong;LI Jian;LI Hao;LIU Yuan-guang(Department of Urology,Zhoukou Central Hospital,Zhoukou 466000;Department of Urology,First Affiliated Hospital of Zhengzhou University,Zhengzhou 450052,China)

机构地区：[1]周口市中心医院泌尿外科,河南周口466000 [2]郑州大学第一附属医院泌尿外科,河南郑州450052

出　　处：《现代泌尿外科杂志》2020年第1期63-67,共5页Journal of Modern Urology

摘　　要：目的探究长链非编码RNA肺腺癌转移相关转录因子1(LncRNA MALAT-1)在肾癌组织及肾细胞癌(RCC)细胞株中的表达情况及其在调控RCC细胞增殖、凋亡及侵袭过程中的作用机制。方法利用实时荧光定量聚合酶链反应(qRT-PCR)实验检测正常和RCC组织以及HK-2、786-O、ACHN及Caki-1细胞中MALAT-1的表达情况;将786-O细胞随机分为3组,分别转染MALAT-1-siRNA沉默载体(si-MALAT-1组)及MALAT-1-siRNA阴性表达载体(si-NC组),空白对照组加入PBS(Blank组)。采用CCK-8法、流式细胞术法、Transwell法检测细胞增殖、凋亡及侵袭能力;利用Western blot法检测Zeste基因同源物增强子2(EZH2)及β-catenin的蛋白表达水平。结果与正常组织及细胞株HK-2相比,肾癌组织及细胞株786-O、ACHN及Caki-1中MALAT-1的表达水平明显增加(P<0.05);与Blank组和si-NC组相比,si-MALAT-1组RCC细胞活性和侵袭能力明显降低、细胞凋亡率明显增加、EZH2及β-catenin的蛋白表达水平明显升高(P<0.05)。结论LncRNA MALAT-1在肾癌组织及RCC细胞中表达上调;抑制MALAT-1的表达能够抑制RCC细胞的增殖和侵袭,促进凋亡,其机制可能与下调EZH2-β-catenin信号通路的表达有关。Objective To investigate the expression of long-chain non-coding RNA MALAT-1(LncRNA MALAT-1)in tissues and cell lines of renal cell carcinoma(RCC)and its mechanism in regulating the proliferation,apoptosis and invasion of RCC cells.Methods The expression of MALAT-1 in heathy tissues,RCC tissues,HK-2,786-O,ACHN and Caki-1 cells were detected with qRT-PCR.The 786-O cells were randomly divided into 3 groups:MALAT-1-siRNA silencing vector group(si-MALAT-1 group),MALAT-1-siRNA negative expression vector group(si-NC group)and blank control group(blank group).The cell proliferation,apoptosis and invasion abilities were detected with CCK-8 method,flow cytometry and Transwell,respectively.The protein expression levels of EZH2 andβ-catenin were detected with Western blot.Results Compared with healthy tissues and HK-2 cell line,RCC tissues,786-O,ACHN and Caki-1 had significantly higher expressions of MALAT-1(P<0.05).Compared with the blank and si-NC groups,the si-MALAT-1 group had significantly decreased activity and invasion ability of RCC cells,but significantly increased apoptosis rate,and increased protein expressions of EZH2 andβ-catenin(P<0.05).Conclusion LncRNA MALAT-1 is up-regulated in RCC cells and tissues.Inhibition of MALAT-1 expression can inhibit the proliferation and invasion of RCC cells and promote the apoptosis.The mechanism may involve the down-regulation of EZH2-β-catenin signaling pathway.

关 键 词：肾细胞癌 MALAT-1 增殖和凋亡 细胞侵袭 EZH2-β-catenin信号通路 

分 类 号：R692[医药卫生—泌尿科学]