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WDR63 inhibits Arp2/3-dependent actin polymerization and mediates the function of p53 in suppressing metastasis

Kailiang Zhao1, Decai Wang2, Xiaolong Zhao2

  • 1The First Affiliated Hospital of USTC, The CAS Key Laboratory of Innate Immunity and Chronic Disease, Hefei National Laboratory for Physical Sciences at Microscale, Division of Lifesciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.

EMBO Reports
|March 5, 2020
PubMed

Insights

The tumor suppressor p53 suppresses cancer metastasis by upregulating WDR63. WDR63 inhibits actin polymerization via the Arp2/3 complex, thereby reducing cell migration and invasion.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • p53 is a tumor suppressor involved in cancer metastasis.
  • Actin dynamics and Arp2/3 complex are crucial for cell migration during metastasis.
  • The precise mechanism of p53's metastasis suppression is not fully understood.

Purpose of the Study:

  • To investigate the role of WDR63 in p53-mediated suppression of cancer metastasis.
  • To elucidate the mechanism by which WDR63 affects cell migration and metastasis.

Main Methods:

  • WDR63 expression analysis.
  • Cell migration and invasion assays.
  • Mouse xenograft models.
  • Co-immunoprecipitation assays to study protein interactions.

Main Results:

  • p53 transcriptionally upregulates WDR63.
  • WDR63 inhibits cell migration, invasion, and metastasis.
  • WDR63 interacts with the Arp2/3 complex and suppresses Arp2/3-mediated actin polymerization.
  • WDR63 overexpression counteracts metastasis promotion caused by p53 depletion.

Conclusions:

  • WDR63 acts as a downstream mediator of p53 in suppressing cancer metastasis.
  • WDR63 regulates Arp2/3 complex function, inhibiting actin polymerization and cell migration.
  • WDR63 is a critical component of the p53 pathway controlling metastasis.
Keywords:
Arp2/3WDR63metastasisp53

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