Cancer therapy: can the challenge be MET?

Abstract

The deregulation of tyrosine kinase receptors (RTKs) is frequent in human tumors and is often associated with the acquisition of an aggressive phenotype. The Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection from apoptosis. The deregulated activation of Met is crucial not only for the acquisition of tumorigenic properties but also to achieve an invasive phenotype. The involvement of MET in human tumors has been definitively established and can be achieved through several mechanisms, including MET interaction with unrelated membrane receptors, such as integrins, plexins, CD44, FAS and other RTKs. Interfering with Met activation is thus a new and challenging approach to hamper tumorigenic and metastatic processes.

• Authors: Simona Corso, Paolo M Comoglio, Silvia Giordano
• Journal: Trends in molecular medicine (Trends Mol Med) Vol. 11 Issue 6 Pg. 284-92 (Jun 2005) ISSN: 1471-4914 [Print] England
• PMID: 15949770 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Cell Adhesion Molecules
• Hyaluronan Receptors
• Nerve Tissue Proteins
• plexin
• Hepatocyte Growth Factor
• Proto-Oncogene Proteins c-met

Topics

• Animals
• Apoptosis
• Cell Adhesion
• Cell Adhesion Molecules (metabolism)
• Hepatocyte Growth Factor (metabolism)
• Humans
• Hyaluronan Receptors (biosynthesis, metabolism)
• Models, Biological
• Neoplasm Invasiveness
• Neoplasms (metabolism, therapy)
• Nerve Tissue Proteins (metabolism)
• Phenotype
• Proto-Oncogene Proteins c-met (physiology)
• Signal Transduction