Long non-coding RNA taurine-upregulated gene 1 promotes cells proliferation, migration and invasion while represses apoptosis, and upregulates AURKA expression in hepatocellular carcinoma

长链非编码RNA牛磺酸上调基因1促进细胞增殖、迁移和侵袭,同时抑制细胞凋亡,并上调肝细胞癌中AURKA的表达。

阅读:2
作者:Peng Kang,Guihua Jiang,Qingyang Meng,Wenjuan Liu,Xia Wu

Abstract

This study aimed to assess the effect of long non-coding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) on cells proliferation, migration, invasion and apoptosis of hepatocellular carcinoma (HCC) cells. LncRNA TUG1 expression was detected in HCC cell lines (SMMC7721, HepG2 and BEL-7402 cells) and normal liver cells (L-02 cells) by qPCR assay. After the transfection of blank mimic, lncRNA TUG1 mimic, blank inhibitor and lncRNA TUG1 inhibitor plasmids into SMMC7721 cells, CKK8, wound-healing, matrigel assay, AV/PI, qPCR assay and western blot assays were performed to detect cells proliferation, migration, invasion, apoptosis, RNA expression and protein expression respectively. LncRNA TUG1 expression was increased in SMMC 7721 cells, HepG2 cells and BEL-7402 cells compared to L-02 cells. After transfection of lncRNA TUG1 mimic and inhibitor plasmids, cells proliferation, migration and invasion were observed to be increased in lncRNA TUG1 mimic group compared to blank mimic group (NC1), while were decreased in lncRNA TUG1 inhibitor group compared with blank inhibitor group (NC2). As to cells apoptosis, AV/PI assay disclosed that lncRNA TUG1 mimic suppressed cells apoptosis rate than NC1 while lncRNA TUG1 inhibitor promoted cells apoptosis rate than NC2, apoptosis markers (C-Caspase3 and Bcl) protein expression also supported the regulation of lncRNA TUG1 on cells apoptosis. In addition, lncRNA TUG1 positively regulated the protein and mRNA expressions of AURKA, but not SERPINE1 or BRAF. In conclusion, lncRNA TUG1 promotes cells proliferation, migration and invasion while represses apoptosis, and upregulates AURKA expression in HCC cells.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。