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[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。
[Objective] To investigate the effect of curcumin on TGF-β-induced epithelial-mesenchymal transition, invasion and metastasis of lung cancer A549 cells and its possible mechanism. [Methods] Transforming growth factor (TGF-β1) was used to induce epithelial-mesenchymal transition in lung cancer cell line A549. Curcumin was used to intervene TGF-β1 -induced lung cancer A549 cells. Morphological changes, cell scratch assay, The invasion and migration of cells were detected by invasion assay. The expressions of E-cadherin, N-cadherin and Vimentin were detected by Western blot and AKT, mTOR phosphorylation in PI3K / AKT / m TOR signal pathway And the effect of curcumin was confirmed by the above method using the PI3K inhibitor LY290004 and the mTOR inhibitor Rapamycin. [Result] Curcumin significantly increased the expression of E-cadherin, inhibited the expression of N-cadherin and Vimentin protein and TGF-β1-stimulated p-AKT and pm TOR in A549 cells compared with the control group, and showed a dose-dependent While inhibiting TGF-β-induced invasion and migration. [Conclusion] Curcumin can significantly inhibit the TGF-β1-induced epithelial-mesenchymal transition of lung cancer A549 cells through PI3K / AKT / m TOR pathway, and reduce the invasion and migration of A549 cells.