中文摘要：

目的 探讨转染Stat3（转录信号传导子和激活子3）显性负性基因Stat3β质粒阻断人结肠癌细胞系SW480细胞的Stat3信号传导通路对人结肠癌细胞增殖和凋亡的影响及可能的机制.方法 应用阳离子脂质体向人结肠癌细胞系SW480细胞中转染携带Stat3β基因的质粒,四唑盐法检测细胞增殖能力,流式细胞术检测细胞周期和细胞凋亡,反转录聚合酶链反应检测Stat3靶基因cyclinD1、bcl-xL mRNA表达情况.数据统计分析采用独立样本t检验.结果 转染Stat3β质粒36 h后,SW480细胞的增殖受到显著抑制（t=5.216,P=0.006）;G0/G1期的细胞比例由40.37%上升至67.25%,S期细胞由44.68%下降至31.23%;发生早期凋亡的细胞比例由5.34%上升至24.42%;同时cyclin D1、bcl-xLmRNA表达水平较对照组显著下降（t=5.228,P=0.010;t=3.517,P=0.025）.结论 转染携带Stat3β基因的质粒可以通过下调Stat3靶基因的表达抑制人结肠癌细胞的增殖,促进凋亡,为以Stat3为靶点的结肠癌基因治疗提供了实验基础.

英文摘要：

Objective To study the influence of transferring a dominant-negative Star3 gene, Star3β on colon cancer cells＇ proliferation and apoptosis in vitro. Methods Cell culture of human colon cancer cell line SW480 and transient transfection were used to evaluate the effect of transferring Star3β to cancer cells. Cell proliferation, cell cycle and apoptosis were quantified by MTT and flow cytometry, respectively. The mRNA expression of Stat3＇s target gene cyclin D1 and bcl-xL was detected by reverse transcription polymerase chain reaction. Independent t tests were used for data statistics. Results 36 h after Stat3β plasmids transfection, proliferation of SW480 cells was significantly inhibited（ t = 5. 216, P = 0. 006） ; cell proportion of GO/GI phase increased from 40. 37% to 67.25% and early apoptosis cells increased from 5.34% to 24. 42% ; mRNA expression of cyclin D1 and bcl-xL declined significantly （t = 5. 288 ,P =0.010;t =3. 517 ,P =0. 025 ）. Conclusion Blocking Stat3 signaling pathway by transfection of Stat3β plasmid inhibits the proliferation and promotes apoptosis of colon cancer cells, which provides a experimental foundation of Stat3 targeted colon cancer gene therapy.