Famitinib enhances nasopharyngeal cancer cell radiosensitivity by attenuating radiation-induced phosphorylation of platelet-derived growth factor receptor and c-kit and inhibiting microvessel formation
Famitinib enhances nasopharyngeal cancer cell radiosensitivity by attenuating radiation-induced phosphorylation of platelet-derived growth factor receptor and c-kit and inhibiting microvessel formation
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DOI：
10.3109/09553002.2015.1062574
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发表时间：
2015-09-01
影响因子：
2.6
通讯作者：
Wu, Gang
中科院分区：
文献类型：
--
作者：
Mu, Xiaoqian;Ma, Jia;Wu, Gang
目的：Famitinib是一种新型酪氨酸激酶抑制剂。本研究通过体内外实验观察法米替尼对人鼻咽癌（NPC）细胞放射敏感性的影响，并探讨其可能的作用机制。材料与方法：人鼻咽癌细胞系（CNE-2）用法米替尼和放射处理，并通过3-（4，5-二甲基噻唑-2-基）-2，5-二苯基四唑溴化物（MTT）、克隆形成存活测定和蛋白质印迹。建立CNE-2细胞移植瘤模型，分析Famitinib和放射对肿瘤体积和微血管密度（MVD）的影响。结果：Famitinib剂量依赖性地抑制CNE-2细胞生长，显著降低克隆形成存活率（P < 0.05）。
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 by 3-(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 microvessel density (MVD).Results: Famitinib dose-dependently inhibited CNE-2 cells growth and significantly reduced clonogenic survival (p