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FOXP3, a novel glioblastoma oncosuppressor, affects proliferation and migration

Véronique Frattini1, Federica Pisati, Maria Carmela Speranza

  • 1Unit of Molecular Neuro-Oncology, Fondazione I.R.C.C.S. Istituto Neurologico C. Besta, Milan, Italy.

Oncotarget
|July 27, 2013
PubMed

Insights

FOXP3, a tumor suppressor, is down-regulated in glioblastoma (GB). Loss of FOXP3 promotes aggressive tumor growth and shorter survival, highlighting its critical role in brain cancer.

Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Molecular Oncology

Background:

  • FOXP3 is crucial for regulatory T cell function and acts as a tumor suppressor in various cancers.
  • FOXP3 expression is altered in glioma, with implications for tumor behavior.

Purpose of the Study:

  • To investigate the role of FOXP3 in glioblastoma (GB) and its potential as a tumor suppressor.
  • To determine the correlation between FOXP3 expression, glioblastoma stem-like cells, and patient survival.

Main Methods:

  • Real-time PCR and immunohistochemistry to assess FOXP3 expression in normal brain, low-grade gliomas, and glioblastomas.
  • In vitro studies involving FOXP3 silencing and overexpression in glioblastoma stem-like cells (GB-NS).
  • Chromatin immunoprecipitation (ChiP) to identify FOXP3 transcriptional targets.

Main Results:

  • FOXP3 is significantly down-regulated in glioblastoma (GB) and GB stem-like cells (GB-NS) compared to normal brain and low-grade gliomas.
  • Lower FOXP3 expression and neurosphere formation in GB correlate with reduced patient survival.
  • FOXP3 silencing enhances GB-NS proliferation, migration, and tumor aggressiveness, while overexpression inhibits these processes.
  • FOXP3 regulates the expression of p21 and c-MYC, key factors in tumorigenesis.

Conclusions:

  • FOXP3 acts as a tumor suppressor in glioblastomas.
  • Down-regulation of FOXP3 contributes to glioblastoma pathogenesis by affecting proliferation, migration, and expression of key oncogenes.
  • Restoring FOXP3 expression may represent a therapeutic strategy for glioblastoma.
Keywords:
FOXP3glioblastomamigrationneurospheresproliferation

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