KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma

Navya Murugesan, Mayinuer Maitituoheti

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.

Original languageEnglish (US)
Article number1984827
JournalMolecular and Cellular Oncology
Volume8
Issue number5
DOIs
StatePublished - 2021

Keywords

  • enhancer reprogramming
  • glycolysis
  • KMT2D
  • melanoma

ASJC Scopus subject areas

  • Molecular Medicine
  • Cancer Research

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