Background and objective: It has been proven that epithelial-mesenchymal transition (EMT) not only correlated with embryonic development but also could promote tumor invasion and metastasis. Transforming growth factor beta-1 (TGF-beta1) has been identified as the main inducer of tumor EMT. The aim of this study was to investigate the effects of TGF-beta1 on EMT and PI3K/AKT signaling pathway in lung adencarcinoma PC9 cells.
Methods: Cultured PC9 cells were treated with different concentrations of TGF-beta1 for 48 h. The morphological changes were observed under phase-contrast microscopy; EMT relative marker protein changes were assessed by Western blot and immunoflurescence staining. In addition, the expression of AKT and P-AKT were also measured by Western blot.
Results: The data showed that TGF-beta1 could induce PC9 morphological alteration from epithelial to mesenchymal and upregulate the expression of mesenchymal maker protein Fibronectin. Obviously, the expression of P-AKT was downregulated by TGF-beta1 treatment for 48 h.
Conclusion: TGF-beta1 might induce EMT of PC9 cells, accompanied by the changes of PI3K/AKT signaling pathway.
背景与目的: 研究表明上皮-间质转化（epithelial-mesenchymal transition, EMT）不仅参与胚胎形成与发育，而且参与肿瘤侵袭转移。此外，人转化生长因子-β1（transforming growth factor-beta1, TGF-β1）已被证实为肿瘤EMT的主要诱导剂。本研究旨在探讨TGF-β1诱导人肺腺癌PC9细胞发生EMT及其对PI3K/AKT信号通道的影响。
方法: 将体外培养的PC9细胞用不同浓度TGF-β1处理48 h，相差倒置显微镜下观察细胞形态学变化；Western blot和细胞免疫荧光验证EMT相关标记蛋白表达变化。同时，采用Western blot方法检测AKT和P-AKT的表达水平。
结果: TGF-β1可诱导PC9细胞向间质型细胞形态转化，并上调间质标记蛋白Fibronectin的表达及下调P-AKT的表达。
结论: TGF-β1可诱导PC9细胞发生EMT，并影响PI3K/AKT信号通道。