What is the stability of CMET (Cell Migration Inducing Protein) expression in CRC (Colorectal Cancer)?

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Last updated: February 15, 2025 • View editorial policy

From the Research

CMET Expression in CRC

  • CMET expression is frequently upregulated in colorectal cancer (CRC) and is associated with invasion and tumor budding 1.
  • The HGF/c-MET axis plays a key role in regulating migration and invasion in CRC, with c-MET activation promoting rapid downregulation of c-MET protein levels 1.
  • cMET overexpression is associated with poor clinical outcomes, including advanced stage cancer and metastasis 2, 3, 4.

Stability of CMET Expression

  • CMET expression is gradually up-regulated in the development and progression of CRC from normal epithelium to adenoma to colorectal carcinoma to metastases 4.
  • High c-MET expression is significantly associated with tumor perineural invasion, gender, and EGFR expression 5.
  • CMET protein expression has a strong correlation with EGFR expression, but KRAS, NRAS, and BRAF gene mutations have no association with c-MET protein levels in primary tumors 5.

Clinical Implications

  • cMET expression may contribute to tumor progression by inhibiting the antioncogene RKIP, providing preclinical justification for targeting RKIP to treat cMET-induced metastasis of CRC 2.
  • cMET immunohistochemistry is significantly higher in primary tumors with perineural invasion, female gender, and EGFR high expression 5.
  • Further studies are required to investigate c-MET as a potential molecular marker of progression and to test the possibility of its incorporation as a new therapeutic target 5.

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