吉西他滨在胰腺癌的放射治疗中增敏机制研究  被引量:6

吉西他滨在胰腺癌的放射治疗中增敏机制研究

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作  者:任宏涛[1] 刁岩[1] 马红兵[1] 王西京[1] 刘蕾[1] 

机构地区:[1]西安交通大学医学院第二附属医院肿瘤科,710004

出  处:《当代医学》2011年第32期1-3,共3页Contemporary Medicine

基  金:西安市科技攻关(GG06187)

摘  要:目的探讨吉西他滨在胰腺癌PC-2细胞体外放疗增敏相关基因谱的影响。方法体外培养胰腺癌PC-2细胞,MTT法检测不同放射剂量(0cGy,50cGy,100cGy,150cGy,200cGy,250cGy)下,不同浓度吉西他滨(空白组,10μg/ml,20μg/ml,30μg/ml,40μg/ml,50μg/ml,60μg/ml,70μg/ml,80μg/ml,90μg/ml及100μg/ml吉西他滨组)对PC-2细胞体外生长的影响。流式细胞仪检测单纯放疗组(空白组,150cGy)和放疗增敏组(40μg/ml吉西他滨,150cGy)对胰腺癌细胞周期及凋亡影响。Human1A基因表达谱芯片分析2组间基因谱差异表达。结果胰腺癌PC-2细胞的凋亡分数与吉西他滨的浓度成剂量依赖关系,在40μg/ml时对PC-2细胞有体外放射增敏作用。对PC-2细胞的G1/S阻滞作用明显,加药放疗组(90.11%)细胞的早期凋亡率较单纯放疗组(71.72%)明显提高。细胞表达谱芯片结果显示,差异表达基因(差异表达两倍以上)共差异表达基因1030条。其中主要包括表达上调的基因348个,下调基因682个。结论吉西他滨主要通过诱导细胞凋亡,抑制细胞周期转化,以及激活肿瘤坏死因子及细胞炎性因子等多种途径阻止放疗间期细胞的修复、杀死瘤细胞发挥其辐射增敏的作用。Objective eDNA micro technology was applied foe screening genes associated with increasing radiate sensitivity by gemcitabine. Methods PC-2 cells were cultured in vitro. The effect different concentrations of gemcitabine on PC-2cells were measured by using MTT methods. Flow cytometry (FCM) was used to measure cell cycle and apoptosis in chemotherapy group. The biostar H-1A gene chip was applied to investigate the differentially expressed genes. Results MTT shows gemcitabine could enhance the radiate sensitivity to PC-2 cells in vitro. FCM showed that the G 1/S stage blocking was caused by 40pg/ml; the rate of apoptosis in control group (71.72%) is lower than the experiment group (90.11%). A total of 1030 genes were expressed differently between two groups,348 up-regulated genes, and down-regulated genes 682. Conclusion Gemcitabine mainly through induction of apoptosis, inhibition of cell cycle transformation, and tumor necrosis factor and the activation of inflammatory factors, and other means to prevent the radiation of cell repair and kill tumor cells to enhance the radiate sensitivity.

关 键 词:胰腺癌 吉西他滨 凋亡 细胞周期 放射治疗 基因表达谱 

分 类 号:R735.9[医药卫生—肿瘤]

 

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