【摘要】 [目的]探讨姜黄素对TGF-β诱导的肺癌A549细胞上皮间质转化、侵袭转移的影响及其可能的机制。[方法]通过转化生长因子TGF-β1诱导肺癌细胞株A549发生上皮间质转化;利用不同浓度姜黄素干预由TGF-β1诱导的肺癌A549细胞,倒置显微镜观察细胞形态变化,细胞划痕实验、Transwell侵袭实验检测细胞迁移及侵袭能力变化,Western blot法检测上皮表型标记蛋白E-cadherin和间质表型标记蛋白N-cadherin、Vimentin的表达及PI3K/AKT/m TOR信号通路中AKT、mTOR磷酸化的情况,并利用PI3K抑制剂LY290004、mTOR抑制剂Rapamycin通过上述方法对姜黄素的作用进行印证。[结果]与对照组相比,姜黄素显著增加A549细胞E-cadherin的表达,抑制N-cadherin和Vimentin蛋白及TGF-β1刺激p-AKT和p-m TOR的表达,且呈明显的剂量—时间依赖关系;同时抑制TGF-β诱导的侵袭迁移。[结论 ]姜黄素可通过PI3K/AKT/m TOR通路明显抑制TGF-β1诱导的肺癌A549细胞上皮间质转化,降低其侵袭迁移能力。更多还原

【Abstract】 [Objective] To investigate the effect of curcumin on TGF-β1-induced epithelial-mesenchymal transition,invasion and migration of lung cancer A549 cells,and the potential mechanism.[Methods] Different concentrations of curcumin were used to intervene the TGF-β1 treated lung cancer A549 cells.The morphological changes were observed under inverted microscope;wound Healing assay and Transwell assay were used to observe the changes if invasion and migration ability of A549 cells;Western blot was used to analyze the expression of epithelial phenotype marker protein E-cadherin,mesenchymal phenotype marker protein N-cadherin,Vimentin and the phosphorylation of transcription factor AKT,mTOR in PI3K/AKT/m TOR signaling pathway.PI3 K inhibitors and m TOR inhibitors were applied to conform the affects of curcumin.[Results]Compared with controls,curcumin inhibited the invasion and migration of TGF-β1-induced A549cell;decreased the expression of N-cadherin,Vimentin;increased the expression of E-cadherin;suppressed the expression of p-AKT and p-m TOR stimulated by TGF-β1,in a dose and time-dependent manner.[Conclusion] Curcumin can inhibit TGF-β1-induced epithelial-mesenchymal transition of lung adenocarcinoma cells,in which PI3K/AKT/m TOR signaling pathway may be involved.更多还原