Long non-coding RNA TMCC1-AS1 predicts poor prognosis and accelerates epithelial-mesenchymal transition in liver cancer

长链非编码 RNA TMCC1-AS1 预测不良预后并加速肝癌上皮-间质转化

阅读:8
作者:Cheng Chen, Na Su, Guiying Li, Yanfeng Shen, Xiaoting Duan

Abstract

Long non-coding RNA transmembrane and coiled-coil domain family 1 antisense RNA 1 (TMCC1-AS1) has been frequently reported to be associated with prognosis in patients with liver cancer (LC). However, the biological role of TMCC1-AS1 in LC in vitro remains unclear. The expression levels of TMCC1-AS1 in primary tumor tissues and LC cell lines were determined using reverse transcription-quantitative PCR. The associations between TMCC1-AS1 expression and the clinicopathological factors of patients with LC were statistically analyzed using the χ2 test. The role of TMCC1-AS1 in LC prognosis was assessed using Kaplan-Meier curves and proportional hazards model (Cox) analysis. Cell proliferation was determined by Cell Counting Kit-8 and colony formation assays. Transwell assays were performed to determine migration and invasion. TMCC1-AS1 expression was found to be significantly upregulated in LC tissues and cell lines compared with the corresponding controls. High TMCC1-AS1 expression was associated with advanced TNM stage and lymph node metastasis. Furthermore, high TMCC1-AS1 expression predicted poor survival in patients with LC. Knockdown of TMCC1-AS1 significantly inhibited the proliferation, migration and invasion of HepG2 and SNU-182 cells, while overexpression of TMCC1-AS1 had the opposite effect in HepG2 and SNU-182 cells. At the molecular level, downregulation of TMCC1-AS1 expression resulted in increased E-cadherin expression and decreased proliferating cell nuclear antigen, Ki67, N-cadherin and Vimentin expression in HepG2 cells. Overexpression of TMCC1-AS1 had the opposite effects on these factors in SNU-182 cells. In conclusion, the present findings indicated that TMCC1-AS1 might be considered as a novel oncogene, which promotes cell proliferation and migration, and may be a potential therapeutic target for LC.

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。