|Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225|
|Liu, Feng1; Wang, Jun-Jie1; You, Zhen-Yu1; Zhang, Ying-Dong1; Zhao, Yong2|
|关键词||EGFR inhibitor Prostate cancer cells Cell proliferation Apoptosis|
|刊名||UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS|
|WOS标题词||Science & Technology|
|类目[WOS]||Oncology ; Urology & Nephrology|
|研究领域[WOS]||Oncology ; Urology & Nephrology|
|关键词[WOS]||GROWTH-FACTOR RECEPTOR ; MODULATED RADIATION-THERAPY ; ACTIVATED PROTEIN-KINASE ; SURVIVIN EXPRESSION ; MAPK PATHWAY ; LUNG-CANCER ; NECK-CANCER ; COMBINATION ; APOPTOSIS ; BINDING|
Purpose: To determine the direct effects of the epidermal growth factor receptor (EGFR) inhibitor C225 on the radiosensitivity of human prostate cancer cells.
Experimental design: Human prostate cancer DU145 cells were irradiated with (60)Co (1.953 Gy/min) at various doses in the presence or absence of C225. The cellular proliferation and cell-survival rate were evaluated by MTT and colony-forming assays after irradiation. The cell-cycle distribution, cell apoptosis, and MAPK expression were investigated using FCM. The expression of Cyclin D1, CDK2, CDK4, and Survivin were determined by RT-PCR.
Results: The RBE in the C225 group compared with that in the control group was 1.39. Cells treated with C225 and irradiated at 4 Gy predominantly exhibited GIG, phase arrest and significant decrease in the fraction of cells in the S phase in comparison with those in the control cells, respectively. An evidently higher apoptosis rate on irradiation at 4 Gy was observed in C225-treated cells compared with that in the control cells. Decreased cell proliferation and increased cell death were further supported by the down-regulation of cyclin D1, CDK2, CDK4, and survivin in C225-treated DU145 cells, as determined by RT-PCR. Furthermore, C225 significantly inhibited the phosphorylation of P38-MAPK in DU145 cells.
Conclusions: The EGER inhibitor C225 increased the radiosensitivity of DU145 cells through antiproliferative effect, inhibition of clonal growth, G(0)/G(1) phase arrest, apoptosis induction, and inhibition of EGFR-signaling pathways by the down-regulation of MAPK activation. (C) 2010 Published by Elsevier Inc.
|作者单位||1.Peking Univ, Hosp 3, Ctr Canc, Beijing 100871, Peoples R China|
2.Chinese Acad Sci, Inst Zool, State Key Lab Biomembrane & Membrane Biotechnol, Transplantat Biol Res Div, Beijing, Peoples R China
|Liu, Feng,Wang, Jun-Jie,You, Zhen-Yu,et al. Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225[J]. UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS,2010,28(1):59-66.|
|APA||Liu, Feng,Wang, Jun-Jie,You, Zhen-Yu,Zhang, Ying-Dong,&Zhao, Yong.(2010).Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225.UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS,28(1),59-66.|
|MLA||Liu, Feng,et al."Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225".UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS 28.1(2010):59-66.|