Sodium glycididazole enhances the radiosensitivity of laryngeal cancer cells through downregulation of ATM signaling pathway
Sodium glycididazole enhances the radiosensitivity of laryngeal cancer cells through downregulation of ATM signaling pathway
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DOI：
10.1007/s13277-015-4278-1
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发表时间：
2016-05-01
期刊：
影响因子：
--
通讯作者：
Wu, Rong
中科院分区：
文献类型：
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作者：
Zeng, Yue-Can;Xing, Rui;Wu, Rong
本研究旨在探讨甘氨双唑钠对喉癌细胞的辐射增敏作用及其机制。两种喉癌细胞系（Hep-2和UT-SCC-19 A）在存在或不存在甘氨双唑钠的情况下用X射线照射。检测细胞存活率、DNA损伤与修复、细胞凋亡、细胞周期分布、细胞周期检查点相关蛋白表达及细胞凋亡。与单纯照射组相比，甘氨双唑钠联合照射组DNA损伤明显增加，G1期细胞减少，G2/M期细胞阻滞，DNA修复蛋白XRCC 1灶形成减少，细胞凋亡增加。联合治疗下调共济失调-毛细血管扩张突变（ATM），p-ATM，CHK 2和P53的蛋白表达，但上调MDM 2和Cdk 2的蛋白表达。本研究表明甘氨双唑钠在体内外均通过下调ATM信号通路增强喉癌细胞的放射敏感性。
The purpose of this study was to evaluate the radiation-enhancing effect of sodium glycididazole, and the corresponding mechanisms of action on laryngeal cancer cells. Two laryngeal cancer cell lines (Hep-2 and UT-SCC-19A) were irradiated with X-rays in the presence or absence of sodium glycididazole. Cell survival, DNA damage and repair, cell apoptosis, cell cycle distribution, expression of proteins related to cell cycle checkpoint, and apoptosis were measured. Significantly increased DNA damages, decreased cells in the G1 phase, arrested cells at G2/Mphase, decreased DNA repair protein XRCC1 foci formation, and enhanced cell apoptosis were observed in laryngeal cell lines treated by sodium glycididazole combined with irradiation compared with the irradiation alone. The combined treatment downregulated the protein expressions of ataxia-telangiectasia mutated (ATM), p-ATM, CHK2, and P53 but upregulated the protein expressions of MDM2 and Cdk2. This study indicates that sodium glycididazole enhances the radiosensitivity of laryngeal cancer cells through downregulation of ATM signaling pathway in vitro and in vivo.