Modulation of c-Met signaling and cellular sensitivity to radiation: potential implications for therapy.

Abstract:

:The c-Met/hepatocyte growth factor receptor and its family members are known to promote cancer cell migration and invasion. Signaling within and beyond this pathway contributes to the systemic spread of metastases through induction of the epithelial-mesenchymal transition, a process also implicated in mediating resistance to current anticancer therapies, including radiation. Induction of c-Met has also been observed after irradiation, suggesting that c-Met participates in radiation-induced disease progression through the epithelial-mesenchymal transition. Therefore, c-Met inhibition is an attractive target for potentially mitigating radiation resistance. This article summarizes key findings regarding crosstalk between radiotherapy and c-Met and discusses studies performed to date in which c-Met inhibition was used as a strategy to increase cellular radiosensitivity.

journal_name

Cancer

journal_title

Cancer

authors

Bhardwaj V,Cascone T,Cortez MA,Amini A,Evans J,Komaki RU,Heymach JV,Welsh JW

doi

10.1002/cncr.27965

subject

Has Abstract

pub_date

2013-05-15 00:00:00

pages

1768-75

issue

10

eissn

0008-543X

issn

1097-0142

journal_volume

119

pub_type

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