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Updated: May 9, 2026

10:37
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Par6 is phosphorylated by aPKC to facilitate EMT
Adrian Gunaratne1, Gianni M Di Guglielmo
1Department of Physiology and Pharmacology; Western University; London, ON, Canada.
Cell Adhesion & Migration
|July 25, 2013
Summary
Polarity proteins Par6 and atypical protein kinase C (aPKC) drive epithelial to mesenchymal transition (EMT) in cancer. Their phosphorylation of Par6 promotes cell migration and invasion, highlighting a role in oncogenic progression.
Area of Science:
- Cell Biology
- Oncology
- Molecular Biology
Background:
- Conserved polarity proteins Par6 and atypical protein kinase C (aPKC) regulate cell polarization.
- Emerging evidence links these proteins to oncogenic progression and cancer development.
- Epithelial to mesenchymal transition (EMT) is crucial for tumor cell migration and invasion.
Purpose of the Study:
- To investigate the role of aPKC in phosphorylating Par6 and driving EMT.
- To understand the implications of Par6 phosphorylation in non-small cell lung cancer (NSCLC) cell migration.
- To explore the link between polarity proteins and cancer progression.
Main Methods:
- Investigated TGFβ-induced phosphorylation of Par6 in epithelial cells.
- Examined aPKC-mediated phosphorylation of Par6 in NSCLC cells.
- Assessed the impact of Par6 phosphorylation on cell migration and invasive potential.
Main Results:
- Par6 phosphorylation by TGFβ leads to junction dissolution, cytoskeletal changes, and increased metastatic potential in epithelial cells.
- aPKC phosphorylates Par6, promoting EMT and enhancing migratory potential in NSCLC cells.
- These findings suggest aPKC as an oncogenic regulator in various tumor types.
Conclusions:
- The aPKC-Par6 pathway is a key driver of EMT and cancer cell migration.
- Targeting this pathway could offer therapeutic strategies for NSCLC and other cancers.
- Understanding polarity protein regulation is vital for both developmental processes and cancer treatment.
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