Long non-coding RNA DILC promotes the progression of gallbladder carcinoma

Gene. 2019 Apr 30:694:102-110. doi: 10.1016/j.gene.2018.12.086. Epub 2019 Feb 1.

Abstract

Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) contribute to tumorigenesis, progression and recurrence of various malignancies including Gallbladder carcinoma (GBC). Lnc-DILC is reported to be the tumor suppressor gene to play an important role in liver cancer stem cells (CSCs). However, the role of lnc-DILC in GBC remains to be elucidated. Herein, we show that lnc-DILC is upregulated in gallbladder CSCs and GBC patients' tissues. Knockdown of lnc-DILC attenuates the self-renewal, tumorigenicity, proliferation and metastasis of gallbladder CSCs. Mechanistically, lnc-DILC promotes gallbladder CSCs expansion via Wnt/β-catenin pathway. Special Wnt/β-catenin inhibitor FH535 diminishes the discrepancy of self-renewal, growth and metastasis between lnc-DILC interference GBC cells and their control cells. In conclusion, lnc-DILC drives gallbladder CSCs self-renewal, tumorigenicity, proliferation and metastasis by activating Wnt/β-catenin signaling, and may therefore prove to be a potential therapeutic target for GBC patients.

Keywords: Cancer stem cell; Gallbladder carcinoma; Lnc-DILC; β-Catenin.

MeSH terms

  • Adult
  • Animals
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation / genetics
  • Cell Transformation, Neoplastic / genetics
  • China
  • Disease Progression
  • Female
  • Gallbladder Neoplasms / genetics*
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Neoplasm Recurrence, Local / genetics
  • Neoplastic Stem Cells / metabolism
  • RNA, Long Noncoding / genetics*
  • RNA, Long Noncoding / metabolism
  • Signal Transduction / genetics
  • Wnt Signaling Pathway / genetics
  • Xenograft Model Antitumor Assays / methods

Substances

  • RNA, Long Noncoding