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. 2018 Sep 27;2(12):1583–1600. doi: 10.1002/hep4.1257

Figure 6.

Figure 6

WNT9A induction by PHB1 silencing is E2F1 dependent. (A) Effect of PHB1 silencing on WNT ligand induction in HepG2 cells. HepG2 cells were forward transfected with NC or PHB1 siRNA for 24 hours and 48 hours. Relative expression of WNT9A, WNT10A, WNT16, and PHB1 was compared to the NC. Results represent mean ± SEM from three independent experiments; #P < 0.001, *P < 0.05 versus NC. (B) Effect of PHB1 and E2F1 cosilencing for 48 hours on WNT9A expression in HepG2 cells. Results represent mean ± SEM from three independent experiments performed in duplicates; #P < 0.001 for siPHB1 versus NC, siPHB1 versus siPHB1+siE2F1. (C) Effect of PHB1 cosilencing with E2F1 overexpression on WNT9A levels in HepG2 cells. Results represent mean ± SEM from three independent experiments performed in duplicates. #P < 0.001 for siPHB1 versus NC, EV versus E2F1 OE, siPHB1 versus siPHB1+E2F1 OE, E2F1 OE versus siPHB1+E2F1 OE. (D) Effect of E2F1 OE for 48 hours in conjunction with 72 hours of PHB1 silencing on phosphorylation of GSK3betaSer9. Data represent two independent experiments. (E) Effect of E2F1 OE for 48 hours in conjunction with 72 hours of PHB1 silencing on CCND1 mRNA levels. Data represent three independent experiments; *P < 0.05 versus NC/EV, #P < 0.05 versus siPHB1 and E2F1 OE. (F) Effect of PHB1 silencing and E2F1 overexpression as in (E) on the expression of anti‐apoptotic protein SURVIVIN in HepG2 cells. Data represent two independent experiments.