Fig 2: EGCG inhibits the PI3K/AKT signal pathway via upregulation of PTEN in TGF-ß1-induced 16HBE cells. (A) Protein expression levels of p-PI3K, PI3K, p-AKT and AKT following treatment of TGF-ß1-induced 16HBE cells with or without EGCG were determined by western blot analysis. Blots underwent semi-quantitative analysis of gray intensity. (B) Relative mRNA expression levels of PTEN in TGF-ß1-induced 16HBE cells, as determined by reverse transncription-quantitative polymerase chain reaction analysis. (C) Protein expression levels of PTEN following treatment of TGF-ß1-induced 16HBE cells with or without EGCG, as determined by western blot analysis. Blots underwent semi-quantitative analysis of gray intensity. Data are presented as the mean ± standard deviation. &&P<0.01 vs. the control group; **P<0.01 vs. the TGF-ß1 group. AKT, protein kinase B; EGCG, epigallocatechin-3-gallate; LY294002, inhibitor of PI3K activity; p-, phosphorylated; PI3K, phosphatidylinositol 3-kinase; PTEN, phosphatase and tensin homolog; TGF-ß1, transforming growth factor-ß1.