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Apical-basal polarity inhibits epithelial-mesenchymal transition and tumour metastasis by PAR-complex-mediated SNAI1

Hae-Yun Jung1, Laurent Fattet1, Jeff H Tsai1

  • 1Department of Pharmacology, Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA.

Nature Cell Biology
|February 27, 2019
PubMed

Insights

Apical-basal polarity suppresses carcinoma metastasis by inhibiting epithelial-mesenchymal transition (EMT). The PAR-atypical protein kinase C (aPKC) complex degrades SNAI1, preventing EMT and invasion.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Carcinoma progression and metastasis are linked to loss of apical-basal polarity and epithelial-mesenchymal transition (EMT).
  • Understanding the regulatory mechanisms controlling EMT is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the role of apical-basal polarity in suppressing EMT and metastatic dissemination.
  • To elucidate the molecular mechanisms by which polarity proteins regulate EMT.

Main Methods:

  • Utilized mouse and human epithelial three-dimensional organoid cultures.
  • Investigated the interaction between the PAR-atypical protein kinase C (aPKC) polarity complex and SNAI1.
  • Analyzed protein phosphorylation and degradation pathways.
  • Examined human breast tumor xenografts and tissue samples.

Main Results:

  • Apical-basal polarity inhibits EMT and invasion by promoting SNAI1 degradation via the aPKC polarity complex.
  • aPKC phosphorylates SNAI1 at S249, leading to its degradation under intact polarity.
  • Loss of polarity stabilizes SNAI1, promoting EMT and invasion.
  • Inhibition of PAR-complex-mediated SNAI1 degradation increases tumor invasion and metastasis in vivo.
  • Human breast tissues show inverse correlation between PAR3 and SNAI1 protein levels.

Conclusions:

  • Apical-basal polarity acts as a critical checkpoint controlling epithelial-mesenchymal plasticity.
  • The PAR-aPKC-SNAI1 axis is a key regulator of EMT and metastasis suppression.
  • Targeting this pathway may offer novel therapeutic strategies for preventing cancer metastasis.

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