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机构地区:[1]安徽医科大学第一附属医院血液内科,合肥230022 [2]安徽医科大学第一附属医院放疗科,合肥230022
出 处:《安徽医科大学学报》2017年第8期1147-1153,共7页Acta Universitatis Medicinalis Anhui
基 金:国家自然科学基金(编号:81201743);中国教育部博士基金(编号:20123420120008);安徽省博士后科学基金资助项目(编号:2015B053)
摘 要:目的探讨多梳基因蛋白EZH2对鼻腔NK/T淋巴瘤细胞放化疗敏感性的影响。方法采用MTS实验测定NK/T淋巴瘤细胞株SNK6对吉西他滨的半数抑制浓度(IC50),利用线性二次模型拟合测定干扰EZH2对SNK6细胞的放疗增敏比(SER);通过流式细胞仪Annexin V/PI双染检测细胞凋亡,并用Western blot法检测凋亡蛋白caspase-3和PARP的断裂带的水平;用免疫荧光检测EZH2干扰后对放射引起的DNA损伤的影响。结果干扰EZH2降低吉西他滨的IC50约为2.54倍,并提高吉西他滨药物引起的凋亡。沉默EZH2能够提高SNK6细胞的放疗敏感性,SER=5.855;提高射线引起的细胞凋亡,并增加细胞凋亡蛋白断裂带的产生;增加射线诱导的DNA损伤。结论 EZH2可以提高NK/T淋巴瘤细胞的放化疗敏感性。Objective To investigate the effect of EZH2 on chemoradiotherapy sensitivity of NK / T lymphoma cells. Methods MTS assay was used to determine the gemcitabine IC50 of SNK6 cell line. Apply linear quadratic model tovalue SER of SNK6 cells. Annexin V/PI double staining was used to detect apoptosis. Western blot was used to measure the amount of cleaved band of caspase-3 and PARP protein. Immunofluorescence was applied to confirm the influenceon DNA damage induced by irradiation. Knockingdown EZH2 decreased the IC50 ofgemcitabine about 2. 54 times when compared with control cells,and it also increased the apoptosis induced by gem-citabine. Silence the express of EZH2 improved the radio sensitivity of SNK6 cell line, the sensitization enhance-ment ratio was 1. 659. It also enhanced the apoptosis caused by IR, and it increased the amount of apoptosis pro-tein induced by IR. Conclusion Suppress the express of EZH2 can improve the radiation and chemotherapy sensi-tivity of NK/T lymphoma cell.
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