反义Stat3基因诱导喉癌细胞凋亡的线粒体机制探讨

Mitochondrial mechanisms of antisense oligodeoxynucleotide Stat3 induced apoptosis in laryngeal carcinoma cell

目的:探讨Stat3反义寡脱氧核苷酸转染人喉癌Hep-2细胞株后,细胞内线粒体的改变,为阐明喉癌细胞凋亡的机制奠定一定的理论基础,为临床上喉癌的治疗开辟一条新思路。方法:将设计好的Stat3反义寡核苷酸序列(ASODN),应用脂质体转染法以不同浓度转染人喉癌Hep-2细胞,并设空白组(MOCK)及正义对照组(SODN)作为比较,检测各转染组Hep-2细胞中线粒体膜电势、电压依赖性阴离子通道(VDAC)以及Cyt-c,以判断线粒体的变化。结果:随着ASODN浓度的增加,线粒体膜电势降低,VDAC逐渐增加,Cyt-c释放逐渐增多。结论:在Stat3影响人喉癌Hep-2细胞凋亡的机制中,线粒体途径发挥了作用。初步阐明Stat3影响喉癌细胞增殖的调控机制,为临床治疗提供了新的研究靶点。

Objective：To investigate the changes of mitochondrion by transferring antisense oligodeoxynucleotide Stat3 into laryngeal cacinoma Hep-2 cell,for elucidating the mechamism of laryngeal carcinoma Hep-2 cell apoptosis,for developing more effective treatment for laryngeal cancer.Method：The designed Stat3 ASODN was transferred into laryngeal cacinoma Hep-2 cell by lipofection.Mitochondrion membrane potential,VDAC and Cyt-c were detected for determining the changes of mitochondrion.Result：MMP was fell,Cyt-c and VDAC were increased with the heighten concentration of ASODN.Conclusion：Mitochondria approach play an important role in the apoptosis mechanism of human Hep-2 cell by Stat3.This research elucidated the regulating mechanism of Hep-2 cell proliferation by Stat3,provided a new research focus for clinical therapy.