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Downregulation of Ezh2 methyltransferase by FOXP3: new insight of FOXP3 into chromatin remodeling?

Zhu Shen1, Ling Chen, Xiaojun Yang

  • 1Department of Dermatology, Southwest Hospital, Third Military Medical University, Chongqing, China. zhushencq@gmail.com

Biochimica Et Biophysica Acta
|May 22, 2013
PubMed

Insights

Transcription factor FOXP3 (forkhead box P3) suppresses breast cancer by reducing Ezh2 levels. FOXP3 accelerates Ezh2 degradation, impacting epigenetic regulation and tumor suppressor activity.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Biology

Background:

  • Transcription factor FOXP3 (forkhead box P3) is a key regulator in regulatory T cells.
  • FOXP3 expression is increasingly found in non-lymphoid cells, including cancer cells.
  • FOXP3 regulates cancer-related genes, particularly suppressor genes in breast cancer.

Purpose of the Study:

  • To elucidate the mechanisms by which FOXP3 regulates suppressor genes in breast cancer.
  • To investigate the relationship between FOXP3 and Ezh2, a key epigenetic regulator in cancer.
  • To determine if FOXP3 acts as a tumor suppressor in breast cancer.

Main Methods:

  • Correlation analysis between FOXP3 and Ezh2 expression.
  • Assessing the impact of FOXP3 overexpression on Ezh2-mediated cellular functions in T47D cells.
  • Investigating the effect of FOXP3 on Ezh2 protein levels and localization.
  • Examining the role of the polyubiquitination-proteasome pathway and Praja1 in FOXP3-mediated Ezh2 downregulation.

Main Results:

  • An inverse correlation was observed between FOXP3 and Ezh2 levels.
  • FOXP3 overexpression inhibited Ezh2's enhancement of mammosphere formation, proliferation, migration, and colony formation in T47D cells.
  • FOXP3 downregulates Ezh2 protein levels, dependent on FOXP3 expression amount and nuclear localization.
  • FOXP3 accelerates Ezh2 protein degradation via the polyubiquitination-proteasome pathway by enhancing Praja1 transcription.

Conclusions:

  • FOXP3 acts as an Ezh2 suppressor, providing a novel mechanism for its role in histone modification.
  • FOXP3's ability to downregulate Ezh2 supports its function as a tumor suppressor in breast cancer.
  • These findings offer new insights into epigenetic regulation in breast cancer and potential therapeutic targets.
Keywords:
Ezh2FOXP3H3K27me3HDACPraja1S-phase kinase-associated protein 2SATB1SKP2TranscriptionUbiquitinationenhancer of zeste homolog 2histone deacetylasemiR-101microRNA-101special AT-rich sequence binding protein 1trimethylation of histone H3 lysine 27

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