Peroxisome proliferator-activated receptor γ agonist pioglitazone inhibits β-catenin-mediated glioma cell growth and invasion

Mol Cell Biochem. 2011 Mar;349(1-2):1-10. doi: 10.1007/s11010-010-0637-9. Epub 2011 Jan 9.


Gliomas are the most common primary tumors of the central nervous system. Rapid proliferation and diffuse brain invasion of these tumors are likely to determine the unfavorable prognosis. Recent studies have shown that ligand activation of peroxisome proliferator-activated receptor γ (PPARγ) can induce differentiation and inhibit proliferation of several cancer cells. In this study, we identified pioglitazone, one PPARγ ligand in particular, suppressed human glioma cells proliferation, migration, and induced glioma cells apoptosis. Concomitantly, expression level of β-catenin protein, a key molecule in carcinogenesis, was decreased in glioma cells treated with pioglitazone. Noteworthy, knockdown of β-catenin expression using siRNA technology mimicked the anti-neoplastic potency of pioglitazone. These results indicate that β-catenin is one of the mediators for pioglitazone to suppress glioma cells growth and invasion. Due to its capacity to counteract β-catenin and glioma cell proliferation and migration, pioglitazone represents a promising drug for adjuvant therapy of glioma and other highly migratory tumor entities.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Cell Line, Tumor
  • Cell Migration Assays
  • Cell Movement / drug effects*
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Down-Regulation
  • Glioma / metabolism
  • Glioma / pathology*
  • Humans
  • Neoplasm Invasiveness
  • PPAR gamma / agonists*
  • Pioglitazone
  • RNA Interference
  • Thiazolidinediones / pharmacology*
  • beta Catenin / genetics
  • beta Catenin / metabolism*


  • Antineoplastic Agents
  • PPAR gamma
  • Thiazolidinediones
  • beta Catenin
  • Pioglitazone