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RhoGAPs attenuate cell proliferation by direct interaction with p53 tetramerization domain

Jie Xu1, Xiaolin Zhou, Jilin Wang

  • 1State Key Laboratory for Oncogenes and Related Genes, Division of Gastroenterology and Hepatology, Renji Hospital, Shanghai Institute for Digestive Diseases, Shanghai Jiao-Tong University School of Medicine, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, 145 Middle Shandong Road, Shanghai 200001, China. xujieletter@gmail.com

Cell Reports
|May 21, 2013
PubMed

Insights

The Rho GTPase activation protein ArhGAP11A binds to the tumor suppressor p53, enhancing its activity to induce cell-cycle arrest and apoptosis. This explains why RhoGAP deletions in cancer may impair tumor suppression.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cell Biology

Background:

  • Rho GTPase activation proteins (RhoGAPs) are frequently deleted or downregulated in various cancers.
  • The precise functional roles of RhoGAPs in cancer development remain largely undefined.

Purpose of the Study:

  • To investigate the functional consequences of RhoGAP downregulation in cancer.
  • To elucidate the molecular mechanism by which ArhGAP11A influences cancer pathways.

Main Methods:

  • Co-immunoprecipitation assays to assess protein interactions.
  • Cell-cycle analysis and apoptosis assays.
  • Western blotting and quantitative PCR to evaluate protein and gene expression.

Main Results:

  • ArhGAP11A directly binds to the tumor suppressor p53, specifically interacting with its tetramerization domain.
  • This interaction stabilizes p53's tetrameric form, enhancing its DNA-binding capacity and transcriptional activity.
  • ArhGAP11A accumulation in the nucleus upon DNA damage correlates with increased p53-mediated cell-cycle arrest and apoptosis.

Conclusions:

  • ArhGAP11A acts as an inducer of cell-cycle arrest and apoptosis through its interaction with p53.
  • The findings provide a mechanistic link between RhoGAP function and tumor suppression.
  • This study highlights the RhoGAP family as a critical nexus connecting cell migration and proliferation pathways in cancer.

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