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Curr Opin Cell Biol. 2014 Dec;31:98-105. doi: 10.1016/j.ceb.2014.09.008. Epub 2014 Oct 8.

MET, a driver of invasive growth and cancer clonal evolution under therapeutic pressure.

Author information

1
Candiolo Cancer Instiute-FPO (IRCCS), Center for Experimental Clinical Molecular Oncology, 10060 Candiolo, Torino, Italy; Department of Oncology, University of Torino, 10060 Candiolo, Torino, Italy. Electronic address: carla.boccaccio@ircc.it.
2
Candiolo Cancer Instiute-FPO (IRCCS), Center for Experimental Clinical Molecular Oncology, 10060 Candiolo, Torino, Italy; Department of Oncology, University of Torino, 10060 Candiolo, Torino, Italy. Electronic address: antonella.cignetto@ircc.it.

Abstract

The MET oncogene, encoding the hepatocyte growth factor receptor, drives invasive growth, a genetic program largely overlapping with epithelial-mesenchymal transition, and governing physiological and pathological processes such as tissue development and regeneration, as well as cancer dissemination. Recent studies show that MET enables cells to overcome damages inflicted by cancer anti-proliferative targeted therapies, radiotherapy or anti-angiogenic agents. After exposure to such therapies, clones of MET-amplified cancer cells arise within the context of genetically heterogeneous tumors and-exploiting an ample platform of signaling pathways-drive recurrence. In cancer stem cells, not only amplification, but also MET physiological expression, inherited from the cell of origin (a stem/progenitor), can contribute to tumorigenesis and therapeutic resistance, by sustaining the inherent self-renewing, self-preserving and invasive growth phenotype.

PMID:
25305631
DOI:
10.1016/j.ceb.2014.09.008
[Indexed for MEDLINE]

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