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

Area of Science:

• Molecular biology
• Cell biology
• Cancer research

Background:

• Scrib (Scribble) is a tumor suppressor involved in cell polarity and migration.
• Identifying Scrib's binding partners is crucial for understanding its tumor suppressor functions.
• MCC (Mutated in Colorectal Cancer) is a recently identified beta-catenin binding protein.

Purpose of the Study:

• To identify novel binding partners of Scrib.
• To characterize the interaction between MCC and Scrib.
• To investigate the role of MCC in cell migration.

Main Methods:

• Co-immunoprecipitation to identify protein interactions.
• Immunofluorescence microscopy to assess protein colocalization.
• Cell migration assays (e.g., wound healing) to evaluate cell movement.
• Western blotting to assess protein expression and activation states of signaling molecules.

Main Results:

• MCC was identified as a novel binding partner for Scrib.
• MCC interacts with Scrib and the NHERF1/NHERF2/Ezrin complex in a PDZ-dependent manner.
• MCC and Scrib colocalize at the cell membrane in T47D cells.
• Reduced MCC expression impairs cell migration.
• MCC inhibits cell migration independently of Rac1, Cdc42, and PAK activation.

Conclusions:

• MCC is a novel scaffold protein that regulates cell migration.
• MCC interacts with Scrib, beta-catenin, and the NHERF1/2 complex.
• MCC's role in cell migration is distinct from Scrib's in its regulation of Rac1/Cdc42/PAK signaling.