GLTSCR2 contributes to the death resistance and invasiveness of hypoxia-selected cancer cells

FEBS Lett. 2012 Sep 21;586(19):3435-40. doi: 10.1016/j.febslet.2012.07.064. Epub 2012 Jul 28.

Abstract

Tumor hypoxia may be an indicator of poor survival in cancer patients. Thus, an understanding of the molecular mechanism responsible for hypoxic tumor selection is essential to gain further insight into tumor biology. Our aim in this study was to investigate whether hypoxia-responsive GLTSCR2 contributes to death resistance and increased invasiveness of hypoxia-selected glioblastoma cells. We found that repeated hypoxia downregulates p53-upstream regulator, GLTSCR2, which resulted in increased death resistance and invasive potential of glioblastoma cells. Restoration of GLTSCR2 expression suppressed the malignant potential of hypoxia-selected cells. Our results indicate that GLTSCR2 participates in hypoxia-induced malignant potential.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Active Transport, Cell Nucleus
  • Base Sequence
  • Cell Hypoxia
  • Cell Line, Tumor
  • Down-Regulation
  • Gene Knockdown Techniques
  • Glioblastoma / genetics
  • Glioblastoma / metabolism*
  • Glioblastoma / pathology*
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Neoplasm Invasiveness
  • RNA, Small Interfering / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / antagonists & inhibitors
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • NOP53 protein, human
  • RNA, Small Interfering
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • JNK Mitogen-Activated Protein Kinases