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PCDH7 Inhibits the Formation of Homotypic Cell-in-Cell Structure

Chenxi Wang1,2, Ang Chen2, Banzhan Ruan2,3

  • 1School of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.

Frontiers in Cell and Developmental Biology
|May 28, 2020
PubMed

Insights

Protocadherin-7 (PCDH7) inhibits homotypic cell-in-cell (hoCIC) structure formation. This discovery reveals PCDH7 as a novel transmembrane protein that suppresses tumor growth by regulating cell adhesion and actomyosin contractility.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • Homotypic cell-in-cell (hoCIC) structures are associated with tumor development and progression.
  • The molecular mechanisms driving hoCIC formation are not well understood.

Purpose of the Study:

  • To investigate the role of Protocadherin-7 (PCDH7) in hoCIC formation.
  • To elucidate the molecular mechanisms by which PCDH7 influences hoCIC structures and tumor growth.

Main Methods:

  • Analysis of PCDH7 expression in relation to hoCIC formation.
  • Experimental manipulation of PCDH7 levels (overexpression and depletion).
  • Investigation of PCDH7 interactions with PP1α and its effect on pMLC2 phosphorylation and actomyosin activity.

Main Results:

  • PCDH7 expression is negatively correlated with hoCIC formation.
  • PCDH7 overexpression inhibits hoCIC formation, while its depletion enhances it.
  • PCDH7 interacts with and inactivates PP1α, increasing pMLC2 phosphorylation and actomyosin contractility, thereby inhibiting hoCIC formation.
  • PCDH7 promotes anchorage-independent cell growth in a hoCIC-dependent manner.

Conclusions:

  • PCDH7 is identified as the first transmembrane protein that inhibits hoCIC formation.
  • PCDH7 plays a crucial role in suppressing tumor growth by modulating hoCIC structures.
  • PCDH7's mechanism involves regulating intercellular adhesion and actomyosin contractility via the PP1α/pMLC2 pathway.
Keywords:
PCDH7actomyosinadherens junctionscell-in-cell structurepMLC2

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