KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer

Hunain Alam, Ming Tang, Mayinuer Maitituoheti, Shilpa S. Dhar, Manish Kumar, Chae Young Han, Chandrashekar R. Ambati, Samir B. Amin, Bingnan Gu, Tsai Yu Chen, Yu Hsi Lin, Jichao Chen, Florian L. Muller, Nagireddy Putluri, Elsa R. Flores, Francesco J. DeMayo, Laura Baseler, Kunal Rai, Min Gyu Lee

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

Histone methyltransferase KMT2D is frequently mutated in lung tumors, and Alam et al. identify KMT2D as a lung tumor suppressor. KMT2D deficiency induces aberrant metabolic reprogramming via super-enhancer impairment, conferring sensitivity to glycolytic inhibitors in lung cancer with KMT2D-inactivating mutations.

Original languageEnglish (US)
Pages (from-to)599-617.e7
JournalCancer Cell
Volume37
Issue number4
DOIs
StatePublished - Apr 13 2020

Keywords

  • epigenetic modifier
  • glycolysis
  • histone methylation
  • histone methyltransferase
  • inhibitor
  • KMT2D
  • lung cancer
  • metabolism
  • super-enhancer
  • tumor suppressor

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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