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Long noncoding RNA lnc-DILC stabilizes PTEN and suppresses clear cell renal cell carcinoma progression

Han Zhang1, Pengtao Wei1, Wenwei Lv1

  • 1Urology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.

Cell & Bioscience
|October 9, 2019
PubMed
Abstract

Insights

Long noncoding RNA DILC (lnc-DILC) acts as a tumor suppressor in clear cell renal cell carcinoma (ccRCC). Restoring lnc-DILC inhibits ccRCC progression by stabilizing PTEN, offering potential therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in human cancer progression.
  • lncRNA downregulated in liver cancer stem cells (lnc-DILC) acts as a tumor suppressor in liver and colorectal cancers.
  • The role of lnc-DILC in clear cell renal cell carcinoma (ccRCC) remains largely unknown.

Purpose of the Study:

  • To investigate the functional role of lnc-DILC in ccRCC.
  • To elucidate the underlying molecular mechanisms of lnc-DILC in ccRCC.
  • To assess the potential of lnc-DILC as a therapeutic target for ccRCC.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to detect lnc-DILC expression in ccRCC tissues.
  • Overexpression and knockdown experiments to assess ccRCC cell proliferation, migration, and invasion.
  • RNA immunoprecipitation, RNA pull-down, ubiquitination, co-immunoprecipitation, and western blot assays to determine molecular mechanisms.

Main Results:

  • lnc-DILC expression is significantly downregulated in ccRCC tissues and correlates with advanced tumor features and poor prognosis.
  • lnc-DILC suppresses ccRCC cell proliferation, migration, and invasion.
  • lnc-DILC stabilizes the tumor suppressor PTEN by inhibiting its ubiquitination and degradation via interactions with WWP2 and USP11, impacting PTEN-AKT signaling.

Conclusions:

  • lnc-DILC functions as a tumor suppressor in ccRCC by regulating PTEN stability.
  • A novel mechanism involving lnc-DILC, PTEN, WWP2, and USP11 in ccRCC progression is revealed.
  • Restoration of lnc-DILC expression represents a potential therapeutic strategy for ccRCC patients.
Keywords:
PTENUSP11UbiquitinationWWP2

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