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EZH2-mediated epigenetic suppression of SH3BGRL potently inhibits lung cancer progression

Zhiping Liu1, Wen Xu1, Xiansheng Tan1

  • 1Department of Oncology, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

Biochemical and Biophysical Research Communications
|February 25, 2021
PubMed

Insights

SH3BGRL, a gene, is down-regulated in lung cancer, suppressing lung cancer stem cell self-renewal and inhibiting tumor growth. Low SH3BGRL expression indicates poor prognosis, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Lung cancer is a leading cause of cancer mortality globally.
  • Lung cancer stem cells (CSCs) drive tumor recurrence and therapeutic resistance.
  • Mechanisms regulating lung CSC self-renewal are not fully understood.

Purpose of the Study:

  • Investigate the role of SH3BGRL in lung cancer.
  • Determine the molecular mechanisms of SH3BGRL regulation and function.
  • Evaluate SH3BGRL as a prognostic marker and therapeutic target for lung cancer.

Main Methods:

  • Quantitative analysis of SH3BGRL expression in lung cancer tissues versus normal tissues.
  • Chromatin immunoprecipitation (ChIP) assay to assess EZH2 binding to the SH3BGRL promoter.
  • In vitro functional assays to evaluate the impact of SH3BGRL overexpression on lung CSC self-renewal, proliferation, and migration.

Main Results:

  • SH3BGRL expression is significantly down-regulated in lung cancer tissues and inversely correlated with patient outcomes.
  • SH3BGRL is weakly expressed in lung CSCs compared to non-CSCs.
  • EZH2 directly represses SH3BGRL transcription epigenetically.
  • Overexpression of SH3BGRL inhibits lung CSC self-renewal, proliferation, and migration in vitro.

Conclusions:

  • SH3BGRL functions as a tumor suppressor by inhibiting lung CSC self-renewal and tumor progression.
  • EZH2-mediated epigenetic silencing of SH3BGRL contributes to lung CSC maintenance.
  • SH3BGRL represents a promising prognostic biomarker and therapeutic target for lung cancer.
Keywords:
Cancer stem cellEZH2Epigenetic silencingLung cancerSH3BGRL

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