STAT3在肺腺癌细胞中的活化与肺腺癌发生机制的研究

目的：探讨STAT3，CyclinDl，CyclinB1，Bcl-2蛋白在肺癌发病中的作用。方法：采用Western-blot检测人肺腺癌细胞A549和正常人胚肺细胞HELF中STAT3，CyclinD1，CyclinB1，Bcl-2蛋白的表达。结果：①STAT3，CyclinDl，CyclinB1，Bcl-2蛋白在人肺腺癌细胞A549和正常人胚肺细胞HELF中均呈阳性表达，且二者表达均有统计学意义（P〈0．05）；②在人肺腺癌细胞A549中，STAT3蛋白的表达与CyclinD1，Bcl-2蛋白的表达成线性相关，而与CyclinB1蛋白的表达则无明显相关性。结论：STAT3信号转导通路可能通过对下游靶基因CyclinD1，Bcl-2蛋白的调控在肺癌的发生中起着重要的作用，但其具体机制还有待进一步深入研究。

MECHANISM OF ACTIVATION OF STAT3 SIGNAL TRANSDUCTION PATHWAY AND ITS ASSOCIATION WITH LUNG ADENOCARCINOMA CELLS

Objective：To investigate the expression of STAT3,CyclinD1,CyclinB1 and Bcl-2 in lung adenocarcinoma cell A549 and human normal lung cell HELF for understanding the mechanism in lung adenocarcinoma. Method：Western blot was used to determine the protein level of STAT3,CyclinD1,CyclinB1,Bcl-2 in lung adenocarinoma cell A549 and human normal lung cell HELF. Results： （1）The protein level of STAT3 ,CyclinD1, CyclinB1,Bcl-2 were increased in lung adenocarcinoma cell A549 compared with human normal lung cell HELF （P〈0.05）. （2）It was also found that the protein level of CyclinD1, Bcl-2 was in a positive correlation with STAT3 in lung adenoearcinoma cell A549 （P〈0.05）.Conlusion：The study has shown that abnormal activation of STAT3 signaling plays an important role in the carcinogenesis of lung adenocarcinoma by regulating the expression of its target gene such as CyclinD1,Bcl-2,but its possible mechanism needs futher investigating.