Fig. 6

PHF8 promotes EMT and metastasis partly dependent on FIP200-mediated autophagic E-cadherin degradation. a, b Exogenous overexpression of FIP200 reverses effects of PHF8-knockdown on migration and invasion of SMMC-7721 and Huh7 cells (magnification, × 100). c Western-blot analysis of expression of FIP200 and EMT markers in SMMC-7721 and Huh7 cells with co-transfection of shPHF8–1# and HA-FIP200. d, e Western-blot analysis of E-cadherin expression in SMMC-7721 and Huh7 cells with co-transfection of shRNAs (shCtrl or shPHF8–1#) and plasmids (Vector or HA-FIP200), and in HepG2 and SK-Hep-1 cells transfected with PHF8 overexpression and pre-treated by CQ (100 μmol) for 12-h, and subsequently treated by CHX (20 μmol) for indicated time. The protein amount of PHF8 and FIP200 were measured as well. f Schematic representation of the mechanism of PHF8 promotes metastasis by transcriptional regulating expression of SNAI1 and VIM and FIP200-dependent autophagic degradation of E-cadherin. Data were presented as mean ± SD. * P < 0.05, ** P < 0.01