摘要
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 study the mechanism of apoptosis in laryngeal carcinoma cell induced by Stat3 antisense oligodeoxynucleotide (ASODN).Method:The designed Stat3 ASODN was transferred into laryngeal cacinoma Hep-2 cell by lipofection. Expression of Bcl-2,Bax and C-Myc were detected by Western blot and PCR.Result:Western blot and PCR results demonstrated that Stat3 ASODN could significantly increased the expression of Bax and decreased the expression of Bcl-2 and C-Myc when the concentration of antisense oligodeoxynucleotide were heightened.Conclusion:Stat3 ASODN participate in apoptosis by enhancing the expression of Bax and reducing the expression of Bcl-2 and C-Myc.
出处
《临床耳鼻咽喉头颈外科杂志》
CAS
CSCD
北大核心
2010年第4期155-157,共3页
Journal of Clinical Otorhinolaryngology Head And Neck Surgery
关键词
喉肿瘤
反义寡脱氧核苷酸
STAT3
凋亡机制
laryngeal neoplasms
antisense oligodeoxynucleotide
Stat3
apoptosis mechanism