Modulation of c-Met signaling and cellular sensitivity to radiation Potential Implications for Therapy

被引：41

作者：

Bhardwaj, Vikas ^{[1
]}

Cascone, Tina ^{[2
]}

Cortez, Maria Angelica ^{[1
]}

Amini, Arya ^{[1
,3
]}

Evans, Jaden ^{[1
,4
]}

Komaki, Ritsuko U. ^{[1
]}

Heymach, John V. ^{[2
]}

Welsh, James W. ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA

[2] Univ Texas MD Anderson Canc Ctr, Dept Thorac Head & Neck Med Oncol, Houston, TX 77030 USA

[3] Univ Calif Irvine, Med Ctr, Orange, CA USA

[4] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA

来源：

CANCER | 2013年 / 119卷 / 10期

关键词：

c-Met; radiotherapy; DNA damage; clinical targeting; epithelial-mesenchymal transition; HEPATOCYTE GROWTH-FACTOR; FACTOR SCATTER FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; RECEPTOR TYROSINE KINASE; ANGIOGENESIS IN-VITRO; LUNG-CANCER PATIENTS; IONIZING-RADIATION; FACTOR/SCATTER FACTOR; COLORECTAL-CANCER; INVASIVE GROWTH;

D O I：

10.1002/cncr.27965

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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. (c) 2013 American Cancer Society.

引用

页码：1768 / 1775

页数：8

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