Stat3信号传导通路对喉癌细胞G1～S期的调控

目的:探讨Stat3信号传导通路对喉癌细胞G1～S期调控的可能机制.方法:应用阳离子脂质体介导Stat3反义寡核苷酸转染人喉癌Hep-2细胞,阻断其Stat3通路;MTT法检测细胞增殖状态;流式细胞术检测细胞周期;Western blot检测Stat3、磷酸化Stat3、G1期Cyclins、CDKs、p21、p27的表达.结果:转染Stat3反义寡核苷酸后喉癌细胞增殖受抑制,Stat3、磷酸化Stat3、G1期Cyclins、CDKs表达水平下降,p21与p27表达水平上升.结论:Stat3信号传导通路可能通过调节CDK/Cyclin复合物与细胞周期索依赖性激酶抑制因子(CKI)成员之间的平衡而调节喉癌细胞G1～S期转换.

The regulation of Stat3 signal transduction pathway to G1 to S phase of laryngocarcinoma cell

Objective:To show that Stat3 played a key role in the G1 to S phase transition in laryngocarcinoma cells.Method:Human laryngocarcinoma cell lines Hep-2 were transfected with Stat3 antisense oligonucleotide mediated by liposome,MTT assay was used to measure the proliferation,flow cytometry was applied to analyze the cell cycle,and the expressions of Stat3,phosphorylation specific Stat3(tyrosine705),CyclinD1,CyclinE,CDK2,CDK4,CDK6,p21 and p27 were detected by western blot.Result:Hep-2 laryngocarcinoma cell lines expressed constitutively activated Stat3.Antisense oligonucleotide which directed blocked up the translation site resulted in growth inhibition,downregulation of Stat3,p-Stat3,Cyclins and CDKs,and upregulation of p21 and p27.Conclusion:Our findings suggested that Stat3 played an important role in the G1 to S phase transition in laryngocarcinoma cells,Stat3 orchestrated cell cycle by regulating the balance between CDK/Cyclin complex and CKI.