Fig. 7

SCAP upregulation promotes sorafenib resistance through inhibiting AMPK-mediated autophagy signalling in HCC tissues. A Immunoblot analysis of SCAP, p-AMPK, t-AMPK, LC3 and P62 protein expression in HCC tissues (n = 12). B, C Representative images of immunofluorescence staining of p-AMPK/SCAP and P62 proteins in HCC tissues (n = 6). Bar = 100 μm. D Correlation analysis of SCAP protein expression and p-AMPK protein expression (n = 12). E Correlation analysis of SCAP protein expression and LC3-II protein expression (n = 12). F Model for SCAP-regulated sorafenib resistance in HCC. HCC patients with hyperlipidaemia exhibit resistance to sorafenib, possibly because lipid disorders lead to upregulation of SCAP expression, resulting in stimulation of intracellular cholesterol, high synthesis, and increased uptake, which will result in sorafenib resistance in liver cancer through AMPK-mediated autophagy. Silencing SCAP substantially increases sorafenib-induced cell death. Data are the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001. P values were determined by one-way ANOVA in (A) and Pearson’s correlation in (D) and (E)