Long non-coding RNA TMPO-AS1 promotes tumor progression via sponging miR-140-5p in breast cancer

长链非编码 RNA TMPO-AS1 通过吸收乳腺癌中的 miR-140-5p 来促进肿瘤进展

阅读:7
作者:Dandan Zhu, Weize Lv, Xiao Zhou, Yu He, Hongbin Yao, Yinxin Yu, Guodong Zhang, Qingyuan Zhang

Abstract

Long non-coding RNAs (lncRNAs) are involved in carcinogenesis and tumor suppression, and are novel biological tumor regulators. However, the functional roles of lncRNAs and their underlying dysregulation mechanisms in breast cancer are not completely understood. The aim of the present study was to investigate the clinical significance and biological functions of lncRNA TMPO antisense RNA 1 (TMPO-AS1) in breast cancer. TMPO-AS1 levels were measured in human cancer tissues and breast cancer cell lines, and the functional roles of TMPO-AS1 in breast cancer cells were investigated by performing in vitro and in vivo assays. Additionally, luciferase reporter assays were conducted to detect the association between microRNA (miR)-140-5p and TMPO-AS1. TMPO-AS1 expression levels were significantly increased in breast cancer tissues and cell lines compared with adjacent non-cancerous tissues and MCF-10A cells, respectively. In vitro and in vivo studies indicated that TMPO-AS1 knockdown significantly suppressed breast cancer cell viability at 48 and 72 h compared with the small interfering (si)RNA negative control group (NC; siNC). TMPO-AS1 knockdown in vitro inhibited MCF-7 and T47D cell migration and invasion compared with the siNC group. TMPO-AS1 knockdown in metastatic breast cancer cells also decreased metastatic colonization in the mouse lung compared with the short hairpin RNA NC group. Mechanistically, TMPO-AS1 promoted cellular viability and migration as a competing endogenous RNA by sponging miR-140-5p. The results suggested that TMPO-AS1 may serve as a potential therapeutic target in patients with breast cancer.

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。