Effect of low glutamine/glucose on hypoxia-induced elevation of hypoxia-inducible factor-1alpha in human pancreatic cancer MiaPaCa-2 and human prostatic cancer DU-145 cells

Clin Cancer Res. 2005 Jul 1;11(13):4694-700. doi: 10.1158/1078-0432.CCR-04-2530.

Abstract

Purpose and experimental design: Tumor microenvironment is characterized by regions of fluctuating and chronic hypoxia, low extracellular pH, and nutrient depletion. Although it is well known that hypoxia stimulates the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha), the role of low extracellular pH and nutrient depletion on hypoxia up-regulation of HIF-1alpha is not well known. In this study, human pancreatic cancer MiaPaCa-2 and human prostatic cancer DU-145 cells were exposed to hypoxia in the presence or absence of glucose, glutamine, and/or pyruvate.

Results: We observed that low glucose and low glutamine, but not low pyruvate, effectively suppressed the elevation of HIF-1alpha level during hypoxia (0.1-1% oxygen). Deprivation of glutamine or glucose inhibited the accumulation of HIF-1alpha in the presence of MG-132, a protease inhibitor, regardless of oxygen tensions. Data from reverse transcription-PCR analysis revealed that the levels of HIF-1alpha mRNA were not significantly changed at different concentrations of glutamine or glucose under hypoxia. The amount of HIF-1alpha suppression was proportional to protein synthesis inhibition.

Conclusions: Our data suggest that glutamine or glucose deprivation inhibits the accumulation of HIF-1alpha under hypoxic conditions by disrupting translational processes rather than transcriptional or proteasomal degradation processes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blotting, Western
  • Cell Hypoxia
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glucose / pharmacology*
  • Glutamine / pharmacology*
  • Humans
  • Male
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • Proteasome Endopeptidase Complex / metabolism
  • Protein Biosynthesis / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • RNA, Messenger
  • Glutamine
  • Proteasome Endopeptidase Complex
  • Glucose