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目的:探讨反义Stat3基因诱导喉癌细胞凋亡的机制。方法:将设计好的已证实能诱导人喉癌细胞凋亡的Stat3反义寡核苷酸序列,应用脂质体瞬时转染法转染人喉癌Hep-2细胞,应用Western blot、PCR检测Hep-2细胞中Bcl-2,Bax及C-Myc基因及蛋白的表达情况。结果:Western blot和RT-PCR结果显示转染Stat3反义寡核苷酸细胞组,Bax的表达随反义寡核苷酸浓度增加,表达增强,而Bcl-2及C-Myc的表达则减弱。结论:反义Stat3寡核苷酸通过上调Bax,下调Bcl-2及C-Myc基因表达来参与其诱导人喉癌Hep-2细胞凋亡的过程。
Objective: To investigate the mechanism of antisense Stat3 gene in inducing laryngeal carcinoma cell apoptosis. Methods: Stat3 antisense oligonucleotides designed to induce apoptosis in human laryngeal carcinoma cells were transfected into human laryngeal carcinoma Hep-2 cells by lipofectamine. Western blot and PCR The expression of Bcl-2, Bax and C-Myc genes and proteins in Hep-2 cells. Results: The results of Western blot and RT-PCR showed that the expression of Bax increased with the increase of antisense oligodeoxynucleotide and the expressions of Bcl-2 and C-Myc were decreased . CONCLUSION: Antisense Stat3 oligonucleotides are involved in the process of inducing apoptosis in human laryngeal carcinoma Hep-2 cells by up-regulating Bax and down-regulating Bcl-2 and C-Myc gene expression.