Fig. 6.

EPZ5676 inhibits EGFR related or downstream signaling pathway and prevents the phenotype change of HPMCs. a Serum-starved HPMCs were cultured in 2ng/ml TGF-β1 for 36 h with different concentrations of EPZ5676 (0, 1, 5, 10 μM). Cell lysates were subjected to immunoblotting analysis with specific antibodies against p-Src, Src, p-ERK1/2, ERK1/2, p-AKT, AKT or GAPDH. b Expression levels of p-Src, p-ERK1/2 and p-AKT were quantified by densitometry and normalized with Src, ERK1/2 and AKT, respectively. Expression levels of Src, ERK1/2 and AKT were quantified by densitometry and normalized with GAPDH. c Cell lysates were subjected to immunoblotting analysis with specific antibodies against Snail, Slug, α-SMA, E-cadherin and GAPDH. d Expression levels of Snail, Slug, α-SMA and E-cadherin were quantified by densitometry and normalized with GAPDH. e Wound-healing assay of HPMCs treated with TGF-β1 (2 ng/ml) in the presence or absence of EPZ5676 (10 μM). Photomicrographs of migrating cells were taken at 0, 18 and 36 h. f The width of the wound was measured, and the migratory rate was calculated. g The mRNA level of α-SMA, Fibronectin, Vimentin, Collagen type I, III was tested by RT-qPCR in HPMCs with three different treatments. Scale bar = 50μm. Data are means ± sem of 4 samples, *P < 0.05, **P < 0.01, *** P < 0.001, P ≥ 0.05 is not significant (NS)