Fig. 5

POSTN protein can release TGFβ1 by activating αvβ3, thereby activating its own expression and secretion; a WB and its corresponding grayscale calculation were used to identify the protein expression in Hep3B and snu387 cells after up-regulate POSTN expression, followed by using cilengitide to target αvβ3 and SB431542 to inhibit TGFβ1 receptor. b CO-IP pull down experiment showed αvβ3/LTAB complex in Hep3B and snu387 cells as well as up-regulate POSTN expression, followed by using cilengitide to target αvβ3 and SB431542 to inhibit TGFβ1. c AP-2α protein expression was examined by WB experiment after up-regulate POSTN expression, followed by using cilengitide to target αvβ3, SB431542 to inhibit TGFβ1, and rapamycin to inhibit mTOR, ***P < 0.001; d-g Clone Formation (d), Invasion (e), Sphere Formation ability (f), and viability (g) of hepatoma cells were measured after up-regulate POSTN expression, followed by using cilengitide to target αvβ3 and SB431542 to inhibit TGFβ1. Data represent mean + SEM of three independent experiments, the significance between groups were labeled beside the group mark. *P < 0.05, **P < 0.01, ***P < 0.001; h In vivo transplanted xenograft verified that blocking the positive feedback loop formed by POSTN/TGFβ1 with Cilengitide or SB431542 would effectively inhibit the high tumorigenic ability of POSTN in HCC cells, the significance between groups were labeled beside the group mark, ***P < 0.001