lncRNA TINCR facilities bladder cancer progression via regulating miR‑7 and mTOR

Mol Med Rep. 2020 Nov;22(5):4243-4253. doi: 10.3892/mmr.2020.11530. Epub 2020 Sep 22.

Abstract

Long non‑coding RNAs (lncRNAs) have been implicated in various human malignancies, but the molecular mechanism of lncRNA TINCR ubiquitin domain containing (TINCR) in bladder cancer remains unclear. The present study found that the expression of TINCR was significantly increased in bladder cancer tissues and cell lines, when compared with that in adjacent normal tissues and normal urinary tract epithelial cell line SV‑HUC‑1, respectively. Moreover, the high expression of TINCR was associated with tumor metastasis and advanced tumor, node, metastasis stage, as well as reduced overall survival rates of patients with bladder cancer. Further investigation revealed that microRNA (miR)‑7 was negatively mediated by TINCR in bladder cancer cells. Silencing of TINCR expression significantly increased miR‑7 expression and reduced bladder cancer cell proliferation, migration and invasion, while knockdown of miR‑7 expression reversed the inhibitory effects of TINCR downregulation on bladder cancer cells. mTOR was then identified as a target gene of miR‑7 in bladder cancer, and it was demonstrated that overexpression of mTOR reversed the inhibitory effects of miR‑7 on bladder cancer cells. In conclusion, this study suggests that TINCR/miR‑7/mTOR signaling may be a potential therapeutic target for bladder cancer.

MeSH terms

  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Disease Progression
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • MicroRNAs / genetics*
  • Neoplasm Invasiveness
  • Neoplasm Staging
  • RNA, Long Noncoding / genetics*
  • TOR Serine-Threonine Kinases / genetics*
  • Up-Regulation*
  • Urinary Bladder Neoplasms / genetics
  • Urinary Bladder Neoplasms / pathology*

Substances

  • MIRN7 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • TINCR lncRNA, human
  • MTOR protein, human
  • TOR Serine-Threonine Kinases