Cutting Edge: NANOG Activates Autophagy under Hypoxic Stress by Binding to BNIP3L Promoter

J Immunol. 2017 Feb 15;198(4):1423-1428. doi: 10.4049/jimmunol.1600981. Epub 2017 Jan 16.

Abstract

Hypoxia upregulates the core pluripotency factors NANOG, SOX2, and OCT4, associated with tumor aggressiveness and resistance to conventional anticancer treatments. We have previously reported that hypoxia-induced NANOG contributed in vitro to tumor cell resistance to autologous-specific CTL and in vivo to the in situ recruitment of immune-suppressive cells. In this study, we investigated the mechanisms underlying NANOG-mediated tumor cell resistance to specific lysis under hypoxia. We demonstrated the tumor-promoting effect of hypoxia on tumor initiation into immunodeficient mice using human non-small lung carcinoma cells. We next showed a link between NANOG and autophagy activation under hypoxia because inhibition of NANOG decreased autophagy in tumor cells. Chromatin immunoprecipitation and luciferase reporter assays revealed a direct binding of NANOG to a transcriptionally active site in a BNIP3L enhancer sequence. These data establish a new link between the pluripotency factor NANOG and autophagy involved in resistance to CTL under hypoxia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy*
  • Cell Hypoxia*
  • Cell Line, Tumor
  • Chromatin Immunoprecipitation
  • Enhancer Elements, Genetic*
  • Humans
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Mice
  • Mitochondrial Proteins / antagonists & inhibitors
  • Mitochondrial Proteins / genetics*
  • Mitochondrial Proteins / metabolism
  • Nanog Homeobox Protein / metabolism*
  • Promoter Regions, Genetic*
  • RNA Interference
  • Up-Regulation

Substances

  • Membrane Proteins
  • Mitochondrial Proteins
  • Nanog Homeobox Protein
  • Nix protein, mouse