Acidic stress promotes a glioma stem cell phenotype

Cell Death Differ. 2011 May;18(5):829-40. doi: 10.1038/cdd.2010.150. Epub 2010 Dec 3.

Abstract

Malignant gliomas are lethal cancers that display cellular hierarchies with cancer stem cells at the apex. Glioma stem cells (GSCs) are not uniformly distributed, but rather located in specialized niches, suggesting that the cancer stem cell phenotype is regulated by the tumor microenvironment. Indeed, recent studies show that hypoxia and its molecular responses regulate cancer stem cell maintenance. We now demonstrate that acidic conditions, independent of restricted oxygen, promote the expression of GSC markers, self-renewal and tumor growth. GSCs exert paracrine effects on tumor growth through elaboration of angiogenic factors, and low pH conditions augment this expression associated with induction of hypoxia inducible factor 2α (HIF2α), a GSC-specific regulator. Induction of HIF2α and other GSC markers by acidic stress can be reverted by elevating pH in vitro, suggesting that raising intratumoral pH may be beneficial for targeting the GSC phenotype. Together, our results suggest that exposure to low pH promotes malignancy through the induction of a cancer stem cell phenotype, and that culturing cancer cells at lower pH reflective of endogenous tumor conditions may better retain the cellular heterogeneity found in tumors.

Publication types

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

MeSH terms

  • Acidosis
  • Angiogenesis Inducing Agents / metabolism
  • Antigens, Differentiation / metabolism
  • Basic Helix-Loop-Helix Transcription Factors / genetics
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Biomarkers, Tumor / metabolism
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / pathology*
  • Gene Expression Regulation, Neoplastic
  • Glioma / metabolism
  • Glioma / pathology*
  • Glucose Transporter Type 1 / genetics
  • Homeodomain Proteins / metabolism
  • Humans
  • Hydrogen-Ion Concentration
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Nanog Homeobox Protein
  • Neoplasm Transplantation
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology*
  • Nerve Tissue Proteins / metabolism
  • Octamer Transcription Factor-3 / metabolism
  • Oligodendrocyte Transcription Factor 2
  • Phenotype
  • Serpins / genetics
  • Stress, Physiological
  • Transcription, Genetic
  • Tumor Microenvironment / physiology
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Angiogenesis Inducing Agents
  • Antigens, Differentiation
  • Basic Helix-Loop-Helix Transcription Factors
  • Biomarkers, Tumor
  • Glucose Transporter Type 1
  • Homeodomain Proteins
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • NANOG protein, human
  • Nanog Homeobox Protein
  • Nerve Tissue Proteins
  • OLIG2 protein, human
  • Octamer Transcription Factor-3
  • Oligodendrocyte Transcription Factor 2
  • POU5F1 protein, human
  • SERPINB9 protein, human
  • SLC2A1 protein, human
  • Serpins
  • Vascular Endothelial Growth Factor A
  • endothelial PAS domain-containing protein 1