Effect of over-expressed phosphatidylinositol-5 gene on epithelial-mesenchymal transition of lung adenocarcinoma and clinical significance

Objective To observer the effect of phosphatidylinositol-5 (GPC5) on epithelial-mesenchymal transition (EMT) in lung adenocarcinoma cells and to investigate the clinical correlation between the expression of GPC5 and EMT key proteins (E-cadherin, Twist1, Vimentin, N-cadherin) in human lung adenocarcinoma tissues. Methods Luciferase labeled lentivirus-induced GPC5 over-expression was used for in vitro studies in A549 cell line (OE-GPC5) and a negative control group (NC). Western blotting was used to compare the expression level differences in EMT related proteins between the two groups. Immunofluorescent assay was used to detect the expression of E-cadherin and Vimentin in the two groups under the intervention of EMT-induced factor transforming growth factor-β (TGF-β) (10 ng/ml, 36 h). The mRNA expression levels of GPC5, E-cadherin and Vimentin were detected by real-time quantitative PCR in 134 cases of lung adenocarcinoma tissues. The correlation analysis of clinical expression was performed by Pearson method. Results The expression level of E-cadherin in the A549 cell line was up-regulated by over-expressed GPC5 (P=0.008), and the expression levels of Vimentin (P=0.012), N-cadherin (P=0.001) and Twist1 (P=0.001) were down-regulated. The immunofluorescent assay indicated that the E-cadherin green fluorescence intensity in OE-GPC5 group was significantly stronger than in NC group (P=0.020), and the Vimentin green fluorescence intensity in OE-GPC5 group was significantly weaker than in NC group (P=0.001). Pearson correlation analysis showed that the mRNA expression of GPC5 was positively correlated with that of E-cadherin in human lung adenocarcinoma tissues (P=0.007), and negatively with that of Twist1 (P=0.023). Conclusion GPC5 may play a role of tumor suppressor gene by reversing the EMT process of lung adenocarcinoma. Key words: Phosphatidylinositol-5; Epithelial-mesenchymal transition; Lung adenocarcinoma