The coordinated functional expression of epidermal growth factor receptor and c-Met in colorectal carcinoma metastasis.
The process of metastasis is a highly selective, nonrandom process resulting in the clonal selection of a population of cells that is able to detach from the primary tumor, invade and survive in the circulation, arrest, extravasate, and ultimately survive and proliferate in the secondary organ-specific site. Tumor cell interactions with the microenvironment can profoundly influence the survival and proliferation of the cell at a secondary site. The epidermal growth factor receptor (EGFR) and the hepatocyte growth factor receptor (c-Met) are two such receptor tyrosine kinases (RTKs) that have been causally implicated in colorectal carcinoma (CRC) progression and metastasis. Activation of these RTKs can stimulate a number of specific pathways directly effecting tumor cell migration, survival and proliferation. The aberrant regulation of the RTKs is often noted in advanced CRC and its' liver metastases and can significantly effect the metastatic phenotype of tumor cells.
Herynk
M H
MH
Department of Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Radinsky
R
R
D000230:Adenocarcinoma / Q000378:metabolism* / Q000556:secondary; D000818:Animals; D002455:Cell Division; D002465:Cell Movement; D002470:Cell Survival; D015179:Colorectal Neoplasms / Q000378:metabolism* / Q000473:pathology; D018450:Disease Progression; D066246:ErbB Receptors / Q000378:metabolism*; D006801:Humans; D009361:Neoplasm Invasiveness / Q000503:physiopathology; D019859:Proto-Oncogene Proteins c-met / Q000378:metabolism*
D066246:ErbB Receptors; D019859:Proto-Oncogene Proteins c-met