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.
Written by:
Yu H, Li X, Sun S, Gao X, Zhou D. Are you the author?
Department of Radiation Oncology, Peking University First Hospital, Peking University, Beijing, China.
Reference: Biochem Biophys Res Commun. 2012 Oct 26;427(3):659-65.
doi: 10.1016/j.bbrc.2012.09.117
PubMed Abstract
PMID: 23026049
UroToday.com Investigative Urology Section
