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Par6-aPKC uncouples ErbB2 induced disruption of polarized epithelial organization from proliferation control

Victoria Aranda1, Teresa Haire, Marissa E Nolan

  • 1Cold Spring Harbor Laboratory,One Bungtown Road, Cold Spring Harbor, NY 11724, USA.

Nature Cell Biology
|October 25, 2006
PubMed

Insights

Oncogene activation, specifically ErbB2, disrupts epithelial cell polarity by targeting the Par polarity complex. This disruption promotes carcinoma development by affecting glandular organization and preventing apoptosis.

Area of Science:

  • Cell biology
  • Cancer research
  • Molecular oncology

Background:

  • Epithelial cell polarity is crucial for tissue organization and is often lost in carcinoma.
  • The specific oncogenes driving polarity loss in cancer remain largely unidentified.

Purpose of the Study:

  • To identify oncogene targets that disrupt epithelial polarity.
  • To investigate the role of ErbB2 in polarity disruption and its association with the Par polarity complex.

Main Methods:

  • Investigated the interaction between activated ErbB2 and the Par polarity complex components (Par6-aPKC).
  • Assessed the impact of inhibiting the Par6-aPKC interaction on ErbB2-induced disruption of breast epithelial acinar organization and apoptosis.

Main Results:

  • Activated ErbB2 disrupts apical-basal polarity by associating with Par6-aPKC.
  • Inhibiting the Par6-aPKC interaction prevented ErbB2 from disrupting acinar organization and protecting cells from apoptosis.
  • Cell proliferation was not dependent on the ErbB2-Par6-aPKC interaction.

Conclusions:

  • Oncogenes, such as ErbB2, target polarity proteins to disrupt glandular organization.
  • This disruption contributes to carcinoma development by promoting cell survival through apoptosis evasion.

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