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作 者:朱杨[1] 李鹤佳[1] 刘继光[1] 李德超[1] 赵雪莲[1]
机构地区:[1]佳木斯大学口腔医学院口腔颌面外科教研室,黑龙江佳木斯154004
出 处:《口腔医学研究》2014年第9期823-825,共3页Journal of Oral Science Research
基 金:黑龙江省卫生厅课题(编号:2013-218);佳木斯大学青年基金项目(编号:Sq2011-021)
摘 要:目的:研究mtDNA损伤修复蛋白POLG的表达调控与γ射线不敏感的口腔鳞状细胞癌细胞(OSC-5)的凋亡损害的相关性。方法:体外培养OSC-5细胞,并用30Gyγ射线处理,MTT比色法检测OSC-5细胞存活率,RNA干涉技术敲除POLG基因,Western Blot检测POLG和Cleaved-PARP蛋白的表达。结果:30Gyγ射线处理后OSC-5细胞的增殖率为(75.67±4.16)%;si-POLG下调OSC-5细胞POLG蛋白表达水平;si-POLG转染的细胞经γ射线处理后Cleaved-PARP蛋白表达增加,细胞存活率下降(P<0.05)。结论:通过抑制口腔鳞状细胞癌细胞mtDNA损伤修复蛋白POLG能增加对γ射线不敏感的OSC细胞的凋亡损害。Objective: To study the correlation between apoptotic damage ofγ-rays insensitive squamous cell carci- noma(OSC-5) cells and the expression of POLG, amitochondrial DNA repair protein. Methods: OSC-5 cells were cultured in vitro and treated with γ irradiation. OSC cells survival rate was calculated with MTT assay. POLG gene was knockouted by RNA interference. POLG and Cleaved-PARP expression levels were detected by western blot. Results: After OSC-5 cells were irradiated at a dose of 30 Gy, the cell proliferation rate was (75.67±4. 16) %. The level of POLG increased, but higher levels were observed in OSC-5 cells at 12h after irradiation. Be- sides, siRNA down-regulated the corresponding protein expression. Transfection of the siRNAs increased apopto- sis of the irradiated cells (P〈0.05). Conclusion: Inhibiting the mtDNA repair protein POLG could enhance apop- totic damage of 7 irradiation insensitive squamous cell carcinoma cells.
关 键 词:口腔鳞状细胞癌线粒体DNA DNA聚合酶γ
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