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Updated: Sep 29, 2025

Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy
07:20

Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy

Published on: October 18, 2024

638

Histone methyltransferase KMT2C plays an oncogenic role in prostate cancer

Jianpo Lian1, Chengdang Xu1, Xi Chen1

  • 1Department of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200065, China.

Journal of Cancer Research and Clinical Oncology
|March 24, 2022
PubMed
Abstract

Insights

KMT2C is overexpressed in prostate cancer (PCa) and drives tumor growth by regulating CLDN8 and ITGAV. Targeting KMT2C may offer a new therapeutic strategy for PCa patients.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Prostate cancer (PCa) is a significant cause of male morbidity and mortality.
  • Abnormalities in epigenetic modifiers are increasingly recognized as key drivers in PCa development.
  • The specific role of KMT2C, a histone methyltransferase, in PCa remains largely unexplored.

Purpose of the Study:

  • To investigate the potential oncogenic role of KMT2C in prostate cancer.
  • To elucidate the molecular mechanisms by which KMT2C influences PCa progression.

Main Methods:

  • Examined KMT2C expression in prostate cancer tissues.
  • Assessed KMT2C's functional impact on prostate cancer cell proliferation, colony formation, and migration.
  • Utilized RNA-seq and CHIP-qPCR to explore underlying mechanisms and identified CLDN8 and ITGAV as downstream targets.

Main Results:

  • Confirmed KMT2C overexpression in PCa at both transcript and protein levels.
  • KMT2C knockdown significantly inhibited cell viability, colony formation, migration, and in vivo tumor growth (~70%).
  • Identified CLDN8 and ITGAV as key downstream genes regulated by KMT2C, influencing MAPK/ERK and EMT pathways.

Conclusions:

  • KMT2C exhibits an oncogenic role in prostate cancer.
  • Epigenetic regulation of CLDN8 and ITGAV by KMT2C modulates critical tumor-signaling pathways.
  • KMT2C presents a potential therapeutic target for the treatment of PCa.
Keywords:
EMTEpigeneticsKMT2CMAPK/ERK signalingProstate cancer

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