Long non-coding RNA DILC suppresses bladder cancer cells progression

Gene. 2019 Aug 20:710:193-201. doi: 10.1016/j.gene.2019.06.009. Epub 2019 Jun 7.

Abstract

Accumulative researches have demonstrated the critical functions of long non-coding RNAs (lncRNAs) in the progression of malignant tumors, including bladder cancer (BC). Our previous studies showed that lnc-DILC was an important tumor suppressor gene in both liver cancer and colorectal cancer. However, the role of lnc-DILC in BC remains to be elucidated. In the present study, we for first found that lnc-DILC was downregulated in human bladder cancer tissues. Lnc-DILC overexpression suppressed the proliferation, metastasis and expansion of bladder cancer stem cells (CSCs). Mechanically, lnc-DILC suppressed BC cells progression via STAT3 pathway. Special STAT3 inhibitor S3I-201 diminished the discrepancy of growth, metastasis and self-renewal ability between lnc-DILC-overexpression BC cells and their control cells, which further confirmed that STAT3 was acquired for lnc-DILC-disrupted BC cell growth, metastasis and self-renewal. Taken together, our results suggest that lnc-DILC is a novel bladder tumor suppressor and indicate that lnc-DILC inhibits BC progression via inactivating STAT3 signaling.

Keywords: Bladder cancer; Proliferation; STAT3; Self-renewal; lnc-DILC.

MeSH terms

  • Aminosalicylic Acids / pharmacology
  • Benzenesulfonates / pharmacology
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Self Renewal / drug effects
  • Disease Progression
  • Down-Regulation*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Neoplasm Metastasis
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / metabolism
  • RNA, Long Noncoding / genetics*
  • STAT3 Transcription Factor / antagonists & inhibitors
  • STAT3 Transcription Factor / genetics
  • Signal Transduction* / drug effects
  • Urinary Bladder Neoplasms / genetics*

Substances

  • Aminosalicylic Acids
  • Benzenesulfonates
  • NSC 74859
  • RNA, Long Noncoding
  • STAT3 Transcription Factor
  • STAT3 protein, human