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探讨Tat-SmacN7诱导食管癌细胞株EC109和非小细胞肺癌细胞株NCL-H460辐射敏感性的机制。采用体外培养EC109细胞和NCL-H460细胞,实验分为对照组、单纯给药组、单纯照射组和给药联合照射组,用RT-PCR检测CAPS8、CASP9和CASP3的转录水平,Fluorogenic caspase assay试剂盒检测Caspase-3、-8、和-9的活性,ELISA方法检测Caspase活性。结果显示,两种肿瘤细胞在使用Tat-SmacN7联合Caspase的抑制剂z-VAD-fmk后,存活曲线较不使用抑制剂组均有明显上移;Caspase-3、-8、和-9的活性在Tat-SmacN7组明显提高,提示Tat-SmacN7可通过细胞凋亡线粒体途径发挥辐射增敏作用,有望成为一种新的辐射增敏剂。
To investigate the mechanism of Tat-SmacN7-induced esophageal cancer cell line EC109 and non-small cell lung cancer cell line NCL-H460 radiation sensitivity. The EC109 cells and NCL-H460 cells were cultured in vitro. The experiment was divided into the control group, the simple administration group, the simple irradiation group and the administration combined irradiation group. The transcription levels of CAPS8, CASP9 and CASP3 were detected by RT-PCR. Fluorogenic caspase assay reagent The Caspase-3, -8, and -9 activity was detected by Caspase-8 assay and Caspase activity by ELISA. The results showed that the survival curves of two kinds of tumor cells were significantly up-regulated by using Tat-SmacN7 combined with Caspase inhibitor z-VAD-fmk, and the activity of Caspase-3, -8, and -9 In Tat-SmacN7 group was significantly increased, suggesting that Tat-SmacN7 can play a role in radiation mitosis through the apoptotic mitochondrial pathway, is expected to become a new radiation sensitizer.