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Doubles game: Src-Stat3 versus p53-PTEN in cellular migration and invasion

Utpal K Mukhopadhyay1, Patrick Mooney, Lilly Jia

  • 1Department of Biochemistry, Queen's University, Kingston, ON, Canada.

Molecular and Cellular Biology
|August 25, 2010
PubMed

Insights

The oncogenes Src and Stat3 promote cell invasion by suppressing tumor suppressors p53 and PTEN. This balance regulates cellular invasiveness, with Src-Stat3 driving invasion and p53-PTEN inhibiting it.

Area of Science:

  • Cell Biology
  • Oncology
  • Molecular Biology

Background:

  • Src and p53 have opposing roles in cell invasion, with Src promoting invasion and p53 inhibiting it.
  • The precise molecular mechanisms underlying this antagonism and the involvement of other key signaling pathways remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism by which Src and p53 regulate cell invasion.
  • To identify downstream effectors and signaling pathways involved in Src-mediated cell invasion and p53-mediated suppression.

Main Methods:

  • Investigated the roles of Signal transducer and activator of transcription 3 (Stat3), caldesmon, and Phosphatase and tensin homolog (PTEN) in the Src/p53 pathway.
  • Utilized molecular and cellular assays to assess podosome formation, cell invasion, and signaling pathway activation.

Main Results:

  • Stat3 acts as a downstream effector of Src, promoting invasion by suppressing p53 and caldesmon.
  • Enhanced p53 upregulates PTEN, which inhibits Stat3 and Src activity, stabilizing the p53/caldesmon axis and repressing invasion.
  • PTEN's protein phosphatase activity is crucial for negatively regulating the Src/Stat3 pathway and inhibiting podosome formation.

Conclusions:

  • Cellular invasiveness is determined by the balance between pro-invasive oncogenes (Src-Stat3) and anti-invasive tumor suppressors (p53-PTEN).
  • The p53-PTEN tumor suppressor axis counteracts the Src-Stat3 oncogenic pathway to control cell invasion.

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