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Title: c-Met inhibitor SU11274 enhances the response of the prostate cancer cell line DU145 to ionizing radiation

Abstract

Highlights: Black-Right-Pointing-Pointer c-Met inhibition could significantly enhance the radiosensitivity of DU145 cells. Black-Right-Pointing-Pointer The mechanisms of the radiosensitization effect of c-Met inhibition on DU145 cells were also presented in this paper. Black-Right-Pointing-Pointer This is the first study demonstrating the effectiveness of c-Met inhibition on treating HRPC cells with radiotherapy. -- Abstract: Hormone-refractory prostate cancer shows substantial resistance to most conventional therapies including radiotherapy, constitutes a key impediment to curing patients with the disease. c-Met overexpression plays a key role in prostate cancer tumorigenesis and disease progression. Here, we demonstrate that c-Met inhibition by SU11274 could significantly suppress cell survival and proliferation as well as enhance the radiosensitivity of DU145 cells. The underlying mechanisms of the effects of SU11274 on DU145 cells may include the inhibition of c-Met signaling, depolarization of the mitochondrial membrane potential, impairment of DNA repair function, abrogation of cell cycle arrest, and enhancement of cell death. Our study is the first to show the effectiveness of combining c-Met inhibition with ionizing radiation to cure hormone-refractory prostate cancer.

Authors:
; ;  [1];  [1];  [2]
  1. Department of Radiation Oncology, Peking University First Hospital, Peking University, Beijing (China)
  2. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing (China)
Publication Date:
OSTI Identifier:
22210311
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 427; Journal Issue: 3; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
62 RADIOLOGY AND NUCLEAR MEDICINE; APOPTOSIS; CELL CYCLE; DNA REPAIR; HORMONES; INHIBITION; MITOCHONDRIA; NEOPLASMS; PROSTATE; RADIOSENSITIVITY; RADIOTHERAPY; REFRACTORIES

Citation Formats

Yu, Hongliang, Li, Xiaoying, Sun, Shaoqian, Gao, Xianshu, E-mail: xsgao777@hotmail.com, and Zhou, Demin, E-mail: deminzhou@bjmu.edu.cn. c-Met inhibitor SU11274 enhances the response of the prostate cancer cell line DU145 to ionizing radiation. United States: N. p., 2012. Web. doi:10.1016/J.BBRC.2012.09.117.
Yu, Hongliang, Li, Xiaoying, Sun, Shaoqian, Gao, Xianshu, E-mail: xsgao777@hotmail.com, & Zhou, Demin, E-mail: deminzhou@bjmu.edu.cn. c-Met inhibitor SU11274 enhances the response of the prostate cancer cell line DU145 to ionizing radiation. United States. doi:10.1016/J.BBRC.2012.09.117.
Yu, Hongliang, Li, Xiaoying, Sun, Shaoqian, Gao, Xianshu, E-mail: xsgao777@hotmail.com, and Zhou, Demin, E-mail: deminzhou@bjmu.edu.cn. Fri . "c-Met inhibitor SU11274 enhances the response of the prostate cancer cell line DU145 to ionizing radiation". United States. doi:10.1016/J.BBRC.2012.09.117.
@article{osti_22210311,
title = {c-Met inhibitor SU11274 enhances the response of the prostate cancer cell line DU145 to ionizing radiation},
author = {Yu, Hongliang and Li, Xiaoying and Sun, Shaoqian and Gao, Xianshu, E-mail: xsgao777@hotmail.com and Zhou, Demin, E-mail: deminzhou@bjmu.edu.cn},
abstractNote = {Highlights: Black-Right-Pointing-Pointer c-Met inhibition could significantly enhance the radiosensitivity of DU145 cells. Black-Right-Pointing-Pointer The mechanisms of the radiosensitization effect of c-Met inhibition on DU145 cells were also presented in this paper. Black-Right-Pointing-Pointer This is the first study demonstrating the effectiveness of c-Met inhibition on treating HRPC cells with radiotherapy. -- Abstract: Hormone-refractory prostate cancer shows substantial resistance to most conventional therapies including radiotherapy, constitutes a key impediment to curing patients with the disease. c-Met overexpression plays a key role in prostate cancer tumorigenesis and disease progression. Here, we demonstrate that c-Met inhibition by SU11274 could significantly suppress cell survival and proliferation as well as enhance the radiosensitivity of DU145 cells. The underlying mechanisms of the effects of SU11274 on DU145 cells may include the inhibition of c-Met signaling, depolarization of the mitochondrial membrane potential, impairment of DNA repair function, abrogation of cell cycle arrest, and enhancement of cell death. Our study is the first to show the effectiveness of combining c-Met inhibition with ionizing radiation to cure hormone-refractory prostate cancer.},
doi = {10.1016/J.BBRC.2012.09.117},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 427,
place = {United States},
year = {2012},
month = {10}
}