摘要
目的:Wnt信号传导通路的异常激活在肿瘤发生和发展中起着重要的作用,而Axin可以通过参与形成降解复合体下调β-catenin负向调控Wnt通路,抑制肿瘤细胞的恶性生物学行为。本次实验的目的是研究Axin对肺癌细胞迁移能力的影响及可能的途径。方法:在已有野生型Axin质粒的基础上构建了突变型Axin质粒(Axin与β-catenin结合位点剪切突变,用AxinΔβ-ca表示),并向A549细胞中转染野生型Axin和突变型Axin。Western blot法检测转染后Axin和β-catenin的表达。用各转染组细胞进行划痕实验和Tr-answell细胞迁移实验。结果:转染野生型Axin可以明显的下调A549中β-catenin的表达(P<0.01),抑制A549细胞的迁移能力(P<0.01),而转染突变型Axin和空质粒后A549细胞中β-catenin没有明显的变化,细胞的迁移能力未受到明显的影响。结论:体轴抑制因子Axin可以明显的抑制肺癌细胞的迁移能力。而这种作用可能与其负向调控Wnt通路有关。Axin可能成为临床治疗肺癌的新靶点。
Objective：Abnormal activation of the Wnt signaling pathway plays an important role in tumorigenesis and tumor progression, Axin could participate into the formation of the degradation complex and down - regulate β- catenin, negatively regulate Wnt pathway and inhibit the malignant behavior of tumor cells. We aim to study the effect of Axin on lung cancer cell migration. Methods： We constructed Axin mutant （ β - catenin binding site shear mutation,refer as AxinΔβ -ca） on the basis of wild type Axin plasmid. Western blot was used to detect the expression of Axin and β - catenin in each group. Wound assay and transwell were performed to study the change of migration after transfection. Results： Transfection of wild - type Axin down - regulated β - catenin （ P 〈 0.01 ） and inhibited the migration of A549 significantly, but transfection of AxinΔβ - ca could not down - regulate β - catenin and affect the migration of A549 cells. Conclusion： Axin could inhibit the migration of A549 cells, and the effect correlates with the ability of Axin negatively regulating Wnt signaling. Axin may become a new target for clinical treatment of lung cancer.
出处
《现代肿瘤医学》
CAS
2013年第5期977-980,共4页
Journal of Modern Oncology
基金
国家自然科学基金项目(编号:No.81071905)
教育部博士点基金项目(编号:No.20102104110015)
