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STRIPAK components determine mode of cancer cell migration and metastasis

Chris D Madsen1, Steven Hooper2, Melda Tozluoglu3

  • 11] Tumour Cell Biology Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields London WC2A 3LY, UK [2] Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5 2200 Copenhagen N, Denmark.

Nature Cell Biology
|December 23, 2014
PubMed

Insights

The STRIPAK complex, including FAM40A and FAM40B, regulates cell shape and migration by controlling the actomyosin cytoskeleton. Mutations in FAM40B are linked to cancer by altering cell contractility.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Cancer Research

Background:

  • The actomyosin cytoskeleton and its plasma membrane linkage are crucial for cell shape and migration.
  • The STRIPAK complex's role in regulating these processes is not fully understood.

Purpose of the Study:

  • To investigate the role of STRIPAK complex components (FAM40A, FAM40B, STRN3) in regulating the actomyosin cortex.
  • To elucidate the molecular mechanisms by which these components influence cell migration and cancer metastasis.

Main Methods:

  • Identification of STRIPAK components as actomyosin regulators.
  • Biochemical assays to study kinase regulation (MST3/MST4) and protein phosphorylation.
  • Computational modeling, in vitro cell migration assays, and in vivo breast cancer metastasis assays.
  • Analysis of FAM40B mutations in human tumors.

Main Results:

  • FAM40A negatively regulates MST3/MST4 kinases, affecting actomyosin-Ezrin/Radixin/Moesin (ERM) protein co-localization via phosphorylation of PPP1CB/PPP1R14A-D.
  • Co-localization of contractile activity and actin-plasma membrane linkage impacts cell migration speed differently on planar versus confined surfaces.
  • FAM40B mutations in human tumors disrupt PP2A interaction, promoting a contractile phenotype linked to cancer progression.

Conclusions:

  • STRIPAK complex components FAM40A and FAM40B are key regulators of the actomyosin cytoskeleton and cell migration.
  • The interplay between actomyosin contractility and plasma membrane linkage influences cell motility in different environments.
  • FAM40B's oncogenic potential is linked to its ability to drive contractility upon mutation.

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