中文摘要：

目的：前期研究发现转染Axin能抑制A549细胞的增殖能力，本研究目的是探讨Axin抑制A549细胞增殖能力的机制。方法：我们构建了野生型和突变型Axin质粒（Axin与β-catenin结合位点剪切突变）转染A549细胞，并应用GSK-3BsiRNA处理细胞，Westernbolt检测各处理组β-catenin和cyclinD1的变化，MTT检测各处理组细胞增殖能力的变化。结果：转染野生型Axin能够明显地下调β-catenin和cyclin D1（P〈0．01），抑制Wnt通路活性和A549细胞的增殖（P〈0．01），而GSK-3BsiRNA可以阻断Axin的这种功能；转染突变型Axin不能有效的下调Wnt通路或A549细胞的增殖能力。结论：Axin主要是通过负向调控wnt通路抑制A549细胞的增殖。Axin可能成为未来治疗肺癌的新靶点。

英文摘要：

Objective： We found that transfection of Axin could inhibit the proliferation of A549 cells, but the ex- act mechanism is unclear. Methods： We constructed wild - type Axin plasmid, Axin mutant （ β - catenin binding site shear mutation） and GSK- 3β siRNA to treat A549, Western blot was used to detect the expression of β -catenin and cyclin D1. MTT was used to study the change of proliferation. Results： Transfection of wild - type Axin down - regulated β -catenin and cyclin D1 （P 〈 0.05 ） and negatively regulated Wnt pathway and the proliferation of A549. GSK - 3β siRNA could block this function of Axin. Transfection of Axin mutant could not down - regulate Wnt path- way or the proliferation of A549. Conclusion：Axin inhibits the proliferation of 3.549 cells mainly through negatively regulating Wnt signaling. Axin may become a new target for clinical treatment of lung cancer.