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Inhibition of Cdc42 is essential for Mig-6 suppression of cell migration induced by EGF

Xinni Jiang1, MengMeng Niu1, Deshi Chen1

  • 1Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610014, China.

Oncotarget
|June 25, 2016
PubMed

Insights

The adaptor protein Mig-6 suppresses cell migration by inhibiting Cdc42 signaling. This interaction is crucial for Mig-6 function and may be disrupted in cancer progression.

Area of Science:

  • Cell biology
  • Molecular biology
  • Cancer research

Background:

  • The adaptor protein Mig-6 negatively regulates EGF signaling.
  • Mig-6 inhibits cell migration by interacting with ErbB receptors or Cdc42.
  • The precise mechanism of Mig-6 inhibition of Cdc42-mediated cell migration remains unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism by which Mig-6 inhibits cell migration via Cdc42.
  • To investigate the role of specific Mig-6 residues in Cdc42 binding and inhibition.
  • To determine the significance of Mig-6/Cdc42 interaction in cancer progression.

Main Methods:

  • Investigated Mig-6 binding to Cdc42 using biochemical assays.
  • Utilized site-directed mutagenesis to identify key residues in Mig-6 for Cdc42 interaction.
  • Assessed the impact of Mig-6 and Cdc42 manipulation on cell migration and filopodia formation in vitro.
  • Correlated Mig-6 expression levels with cancer progression in patient samples.

Main Results:

  • Mig-6 binding to Cdc42 is necessary and sufficient to inhibit EGF-induced cell migration and filopodia formation.
  • Four specific residues (I11, R12, M26, R30) in the Mig-6 CRIB domain mediate Cdc42 binding and are essential for Mig-6 function.
  • Ectopic expression of Cdc42 rescued Mig-6-mediated inhibition of cell migration.
  • Mig-6's interaction with EGFR is dispensable for inhibiting cell migration.
  • Decreased Mig-6 expression correlates with advanced breast and prostate cancer.

Conclusions:

  • Mig-6 inhibition of Cdc42 signaling is critical for suppressing cell migration.
  • Specific residues in the Mig-6 CRIB domain are essential for this inhibitory function.
  • Disruption of the Mig-6/Cdc42 pathway may contribute to cancer development and progression.
Keywords:
Cdc42EGFMig-6migration

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