Hypoxia-selective macroautophagy and cell survival signaled by autocrine PDGFR activity

Genes Dev. 2009 Jun 1;23(11):1283-8. doi: 10.1101/gad.521709.

Abstract

The selective regulation of macroautophagy remains poorly defined. Here we report that PDGFR signaling is an essential selective promoter of hypoxia-induced macroautophagy. Hypoxia-induced macroautophagy in tumor cells is also HIF1alpha-dependent, with HIF1alpha integrating signals from PDGFRs and oxygen tension. Inhibition of PDGFR signaling reduces HIF1alpha half-life, despite buffering of steady-state protein levels by a compensatory increase in HIF1alpha mRNA. This markedly changes HIF1alpha protein pool dynamics, and consequently reduces the HIF1alpha transcriptome. As autocrine growth factor signaling is a hallmark of many cancers, cell-autonomous enhancement of HIF1alpha-mediated macroautophagy may represent a mechanism for augmenting tumor cell survival under hypoxic conditions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aryl Hydrocarbon Receptor Nuclear Translocator / metabolism
  • Autocrine Communication
  • Autophagy / physiology*
  • Cell Line
  • Cell Line, Tumor
  • Cell Survival
  • Cytosol / metabolism
  • Drosophila melanogaster / metabolism
  • HCT116 Cells
  • Humans
  • Hypoxia*
  • Receptors, Platelet-Derived Growth Factor / metabolism*
  • Signal Transduction*

Substances

  • Aryl Hydrocarbon Receptor Nuclear Translocator
  • Receptors, Platelet-Derived Growth Factor