雷公藤红素上调lncRNA MEG3表达抑制肝癌细胞增殖及促进细胞凋亡  

Celastrol inhibits HepG2 cells proliferation and promotes cells apoptosis by targeting lncRNA MEG3

作　　者：陈晓雷[1] 杨秀丽[1] 周天竹 周梦阳 李新新[1] 张海燕[2] 孟欣[3] Chen Xiaolei;Yang Xiuli;Zhou Tianzhu;Zhou Mengyang;Li Xinxin;Zhang Haiyan;Meng Xin(Institute of Forensic and Judicial Research,Shenyang Medical College,Liaoning Shenyang 110034,China;Department of Geriatrics,the First Affiliated Hospital,China Medical University,Liaoning Shenyang 110001,China;Department of Biochemistry and Molecular Biology,College of Basic Medicine,China Medical University,Liaoning Shenyang 110122,China)

机构地区：[1]沈阳医学院法医司法研究所,辽宁沈阳110034 [2]中国医科大学附属第一医院老年病科,辽宁沈阳110001 [3]中国医科大学基础医学院生化实验室,辽宁沈阳110122

出　　处：《现代肿瘤医学》2019年第5期739-742,共4页Journal of Modern Oncology

基　　金：国家自然科学基金(编号:81572831);沈阳市科技计划项目(编号:17-230-9-27)

摘　　要：目的:探讨MEG3在雷公藤红素诱导的肝癌HepG2细胞凋亡和细胞增殖抑制过程中的作用。方法:采用CCK-8法检测HepG2细胞增殖情况,流式细胞仪检测细胞凋亡情况,Western blot检测cleaved caspase-3、Bax和Bcl-2蛋白的表达,real-time PCR检测MEG3的表达。结果:雷公藤红素抑制HepG2细胞增殖、促进细胞凋亡并上调MEG3的表达;敲低MEG3的表达后显著逆转了雷公藤红素诱导的HepG2细胞增殖抑制和细胞凋亡。结论:雷公藤红素通过上调MEG3的表达抑制HepG2细胞增殖、促进细胞凋亡。Objective:To explore the role of MEG3 in the HepG2 cells apoptosis and cells proliferation induced by celastrol.Methods:CCK-8 was used to detect the proliferation of HepG2 cells.Flow cytometry was used to detect HepG2 cells apoptosis.The expressions of cleaved caspase-3,Bax and Bcl-2 protein were detected by Western blot,and real-time PCR was used to detect the expression of MEG3.Results:Celastrol inhibited the proliferation of HepG2 cells and promoted cells apoptosis by up-regulating the expression of MEG3.After knocking down MEG3 with siRNA,it significantly reversed the proliferation inhibition and apoptosis of HepG2 cells induced by celastrol.Conclusion:Celastrol inhibits HepG2 cells proliferation and promotes cell apoptosis by up-regulating MEG3.

关 键 词：雷公藤红素 长链非编码RNA MEG3 增殖 凋亡 肝癌 

分 类 号：R735.7[医药卫生—肿瘤]