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EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis

Haeun Kim1, Seo Yoon Choi1, Jinyeong Lim2

  • 1Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea.

International Journal of Molecular Sciences
|February 8, 2020
PubMed

Insights

Euchromatic histone-lysine N-methyltransferase 2 (EHMT2) inhibition reduces non-small cell lung cancer (NSCLC) cell viability by impacting cholesterol metabolism and inducing autophagy. This epigenetic targeting offers a novel therapeutic strategy for NSCLC.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) tumorigenesis involves epigenetic alterations.
  • Euchromatic histone-lysine N-methyltransferase 2 (EHMT2) is implicated in various cancers but its role in NSCLC is unclear.
  • EHMT2 catalyzes H3K9 methylation, leading to gene silencing.

Purpose of the Study:

  • To investigate the role of EHMT2 in NSCLC.
  • To explore the therapeutic potential of EHMT2 inhibition in NSCLC.

Main Methods:

  • Analysis of publicly available gene expression data.
  • Inhibition of EHMT2 using BIX01294 (BIX) in NSCLC cell lines.
  • RNA sequencing to identify affected pathways.
  • Assessment of cell viability, autophagy, and cholesterol biosynthesis.

Main Results:

  • EHMT2 expression is elevated in NSCLC tissues.
  • BIX treatment reduced NSCLC cell viability by inducing autophagy.
  • EHMT2 inhibition altered cholesterol biosynthesis pathways, including SREBF2 expression.
  • Cholesterol biosynthesis inhibition partially rescued BIX-induced cell death.

Conclusions:

  • EHMT2 inhibition induces cell death in NSCLC cells.
  • The mechanism involves altered cholesterol metabolism-dependent autophagy.
  • Targeting EHMT2 represents a potential therapeutic strategy for NSCLC.
Keywords:
EHMT2autophagycancer metabolismcholesterol synthesisepigeneticslung cancer

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