Modulation of c‐Met signaling and cellular sensitivity to radiation. Issue 10 (19th February 2013)

• Record Type: Journal Article
• Authors: Bhardwaj, Vikas; Cascone, Tina; Cortez, Maria Angelica; Amini, Arya; Evans, Jaden; Komaki, Ritsuko U.; Heymach, John V.; Welsh, James W.
• Is Part Of: Cancer. Volume 119:Issue 10(2013)
• Page Start: 1768
• Page End: 1775
• Publication Date: 2013-02-19
• Subjects: Cancer -- Periodicals; Cancer -- Cytopathology -- Periodicals; 616.99405
• DOI: 10.1002/cncr.27965
• Languages: English
• ISSNs: 0008-543X

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p>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. Cancer 2013. © 2013 American Cancer Society.</p> </abstract>