Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models

Lillian J. Eichner, Sonja N. Brun, Sébastien Herzig, Nathan P. Young, Stephanie D. Curtis, David B. Shackelford, Maxim N. Shokhirev, Mathias Leblanc, Liliana I. Vera, Amanda Hutchins, Debbie S. Ross, Reuben J. Shaw*, Robert U. Svensson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

81 Scopus citations

Abstract

AMPK can either inhibit or promote tumor growth depending on tumor type and context. Eichner et al. show that AMPK, unlike LKB1, has a pro-tumorigenic role in a Kras-dependent, non-small-cell lung cancer model through the regulation of Tfe3, a master regulator of lysosomes, which supports lung tumor growth.

Original languageEnglish (US)
Pages (from-to)285-302.e7
JournalCell Metabolism
Volume29
Issue number2
DOIs
StatePublished - Feb 5 2019
Externally publishedYes

Keywords

  • AMPK
  • Kras
  • LKB1
  • Tfe3
  • Tfeb
  • cancer
  • lung
  • lysosomes
  • metabolism
  • tumor

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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