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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 intracellular mitochondria after transfection of Stat3 antisense oligodeoxynucleotide into human laryngeal carcinoma Hep-2 cell line, so as to lay a theoretical foundation for elucidating the mechanism of laryngeal carcinoma cell apoptosis, Treatment to open up a new idea. Methods: The designed Stat3 antisense oligonucleotide sequence (ASODN) was transfected into human laryngeal carcinoma Hep-2 cells by lipofection method at different concentrations. Mock and control group SODN) were compared to detect mitochondrial membrane potential, voltage-dependent anion channels (VDAC) and Cyt-c in Hep-2 cells of each transfected group. Results: With the increase of ASODN concentration, the mitochondrial membrane potential decreased, VDAC gradually increased, and Cyt-c release gradually increased. Conclusion: Mitochondrial pathway plays a role in the mechanism of Stat3 affecting the apoptosis of human laryngeal carcinoma Hep-2 cells. To clarify the regulatory mechanism of Stat3 on the proliferation of laryngeal carcinoma cells, it provides a new research target for clinical treatment.