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Related Experiment Video

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STAT3 integrates cooperative Ras and TGF-β signals that induce Snail expression.

M Saitoh1, K Endo1, S Furuya1,2

  • 1Department of Biochemistry, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Japan.

Oncogene
|May 12, 2015
PubMed
Summary

Signal transducer and activator of transcription 3 (STAT3) synergizes transforming growth factor β (TGF-β) and Ras signals to enhance Snail induction, a key event in epithelial tumors.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Epithelial-mesenchymal transition (EMT) is vital in epithelial tumor progression.
  • Transforming growth factor β (TGF-β) induces EMT via Snail, a key regulator.
  • The synergistic mechanism of TGF-β and Ras in Snail induction remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which TGF-β and Ras signals synergize to induce Snail.
  • To identify the role of signal transducer and activator of transcription 3 (STAT3) in this synergistic pathway.

Main Methods:

  • Investigated STAT3's role using overexpression and siRNA knockdown.
  • Utilized STAT3 mutants (YF and transcriptionally inactive) to assess function.
  • Analyzed STAT3-binding elements in Snail promoter regions.
  • Examined the interaction between STAT3, PIAS3, and Smad3.

Main Results:

  • STAT3 overexpression enhanced Snail induction; STAT3 knockdown inhibited it.
  • STAT3's Tyr 705 residue and transcriptional activity are essential for enhancing Snail induction.
  • STAT3-binding elements in the Snail promoter were not required.
  • TGF-β reduced STAT3-PIAS3 interaction and increased PIAS3-Smad3 binding in Ras-activated cells.

Conclusions:

  • STAT3 acts as a mediator, synergizing TGF-β and Ras signals for Snail induction.
  • TGF-β dissociates STAT3 from PIAS3, facilitating STAT3's role in Snail induction.
  • This mechanism highlights a novel pathway regulating EMT in cancer progression.