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. 2017 Aug 2;8(39):66154–66168. doi: 10.18632/oncotarget.19825

Figure 5. EDG2 mediated EMT and Skp2/p27kip1 axis through PI3K/AKT/mTOR signaling.

Figure 5

(A) As detected by Western immunoblotting, enhanced expression of EDG2 leaded to more phosphorylation of AKT and mTOR in Huh7 cells. Consequently, both decreased expression of E-cadherin and increased expression of Vimentin and Fibronectin was found after over-expression of EDG2 in Huh7. Skp2 expression was increased in Huh7 EDG2 cells, while p27kip1 expression was inhibited. However, the PI3K inhibitor LY294002 treatment abrogated the influence of EDG2 on the phosphorylation of mTOR, EMT markers and Skp2/p27kip1 axis. (B) BrdU Incoporation ELISA assay found that LY294002 treatment inhibited the proliferation of both Huh7 EDG2 and Huh7 Vector cells significantly. In addition, LY294002 abolished the pro-proliferation function of EDG2 on Huh7 cells. (C) Knockdown of EDG2 repressed the phosphorylation of both AKT and mTOR, decreased Skp2 expression and up-regulated p27(kip1.