标题：Famitinib enhances nasopharyngeal cancer cell radiosensitivity by attenuating radiation-induced phosphorylation of platelet-derived growth factor receptor and c-kit and inhibiting micro-vessel formati

作者：Mu X, Ma J, Zhang Z, Zhou H, Xu S, Qin Y, Huang J, Yang K, Wu G.

网址:

求助者：01200502

• 求助时间：2015/6/24 8:55:53
• 求助状态：AB图书馆客服已找到全文，详情咨询在线客服qq 1257749646
• 文献摘要：

PURPOSE: Famitinib is a novel tyrosine kinase inhibitor. We investigated the effects of famitinib on the radiosensitivity of human nasopharyngeal carcinoma (NPC) cell radiosensitivity in vitro and in vivo, and explored its possible mechanisms. MATERIALS AND METHODS: Human nasopharyngeal carcinoma cell line (CNE-2) were treated with famitinib and radiation, and analyzed by3-(4,5-dimethylthaizol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), clonogenic survival assay, and western blot. A xenograft model using CNE-2 cells was established to analyze the effects of famitinib and radiation on tumor volume and micro-vessel density (MVD). RESULTS: Famitinib dose-dependently inhibited CNE-2 cells growth and significantly reduced clonogenic survival (p <0.05), with a sensitivity enhancement ratio (SER) of 1.45. The tumor inhibition rate of the combined treatment group was 91%, which was significantly higher than the radiation group (35%, p <0.05) and famitinib group (46%, p <0.05). Famitinib attenuated radiation-induced phosphorylation of the Platelet-derived growth factor receptor (PDGFR) and stem cell factor (c-kit) at 0, 30, 60 min after radiation treatment. Furthermore, radiation combined with famitinib decreased tumor MVD (p <0.05). CONCLUSIONS: Famitinib significantly increased CNE-2 cell radiosensitivity in vitro and in vivo by attenuating radiation-induced PDGFR and c-kit phosphorylation and by inhibiting micro-vessel formation.

文献《Famitinib enhances nasopharyngeal cancer cell radiosensitivity by attenuating radiation-induced phosphorylation of platelet-derived growth factor receptor and c-kit and inhibiting micro-vessel formati》已经找到全文，详情请咨询在线客服 qq 1257749646。
如果您还有其他需要寻找全文的文献，请点击文献求助提交

说明：文献求助是指AB图书馆根据读者的需求，为读者查找论文资料的服务。如果您搜索到相关资料，但不能获取全文，此时便可将有关信息提交求助，由值班客服为您寻找所需文献的全文。提供的文献均来自网络共享资源，不涉及版权交易；如侵犯了您的权利，请告知在线客服，立马删除。文件格式以PDF格式为主。