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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复合物与细胞周期素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。
Objective: To investigate the possible mechanism of Stat3 signaling pathway regulating G1-S phase in laryngeal carcinoma cells. Methods: Stat3 antisense oligonucleotides were transfected into human laryngeal carcinoma Hep-2 cells with cationic liposomes to block the Stat3 pathway. Cell proliferation was detected by MTT assay. Cell cycle was detected by flow cytometry. Stat3, phospho Stat3, G1 phase Cyclins, CDKs, p21, p27 expression. RESULTS: After transfected with Stat3 antisense oligonucleotide, the proliferation of laryngeal carcinoma cells was inhibited. The expressions of Cyclins and CDKs in Stat3, phosphorylated Stat3 and G1 were decreased and the expressions of p21 and p27 were up-regulated. CONCLUSIONS: Stat3 signaling pathway may regulate G1-S transition in laryngeal carcinoma cells by regulating the balance between CDK / Cyclin complex and members of cyclin-dependent kinase inhibitor (CKI).