MCC, a new interacting protein for Scrib, is required for cell migration in epithelial cells

FEBS Lett. 2009 Jul 21;583(14):2326-32. doi: 10.1016/j.febslet.2009.06.034. Epub 2009 Jun 24.

Abstract

To further characterize the molecular events supporting the tumor suppressor activity of Scrib in mammals, we aim to identify new binding partners. We isolated MCC, a recently identified binding partner for beta-catenin, as a new interacting protein for Scrib. MCC interacts with both Scrib and the NHERF1/NHERF2/Ezrin complex in a PDZ-dependent manner. In T47D cells, MCC and Scrib proteins colocalize at the cell membrane and reduced expression of MCC results in impaired cell migration. By contrast to Scrib, MCC inhibits cell directed migration independently of Rac1, Cdc42 and PAK activation. Altogether, these results identify MCC as a potential scaffold protein regulating cell movement and able to bind Scrib, beta-catenin and NHERF1/2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Movement / physiology*
  • Enzyme Activation
  • Epithelial Cells / cytology
  • Epithelial Cells / physiology*
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism
  • Protein Binding
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Sodium-Hydrogen Exchangers / genetics
  • Sodium-Hydrogen Exchangers / metabolism
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • beta Catenin / metabolism
  • cdc42 GTP-Binding Protein / metabolism
  • rac1 GTP-Binding Protein / metabolism

Substances

  • Membrane Proteins
  • Phosphoproteins
  • Recombinant Fusion Proteins
  • SCRIB protein, human
  • Sodium-Hydrogen Exchangers
  • Tumor Suppressor Proteins
  • beta Catenin
  • sodium-hydrogen exchanger regulatory factor
  • MCC protein, human
  • cdc42 GTP-Binding Protein
  • rac1 GTP-Binding Protein