Repository of Research and Investigative Information

Repository of Research and Investigative Information

Baqiyatallah University of Medical Sciences

The c-Met receptor: Implication for targeted therapies in colorectal cancer

(2017) The c-Met receptor: Implication for targeted therapies in colorectal cancer. Tumor Biology. p. 13. ISSN 1010-4283

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Abstract

c-Met (mesenchymal-epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Met receptor could be a promising strategy, in the treatment of colorectal cancer patients. Recently, it was also shown that crosstalk between c-Met and other cell surface receptors attributes to tumorigenesis and development of therapeutic resistance. Characterization of the molecular mechanisms through which c-Met crosstalks with other receptors in favor of tumor formation and progression remains to explore. This review will describe the mechanisms of aberrant c-Met signaling in colorectal cancer and discuss on additional roles for c-Met receptor through crosstalk with other tyrosine kinase receptors and cell surface proteins in colorectal cancer. Novel therapeutic approaches for c-Met pathway targeting will also be discussed.

Item Type: Article
Keywords: c-Met hepatocyte growth factor colorectal cancer crosstalk targeted therapies hepatocyte growth-factor primary colon-cancer cell lung-cancer tyrosine kinase somatic mutations gastric-cancer antitumor-activity signaling pathway hgf/c-met hepatocellular-carcinoma Oncology
Divisions:
Page Range: p. 13
Journal or Publication Title: Tumor Biology
Journal Index: ISI
Volume: 39
Number: 5
Identification Number: https://doi.org/10.1177/1010428317699118
ISSN: 1010-4283
Depositing User: مهندس مهدی شریفی
URI: http://eprints.bmsu.ac.ir/id/eprint/4421

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