Fig. 1
Glucose availability induces PCSK9 expression in HepG2-xenografts. a Intraperitoneal glucose tolerance test (GTT) in mice from group I and group II. b Tumor progression in group III and group IV, after injecting HepG2 cells (5 × 106) subcutaneously. c Individual serum samples collected from group III and group IV were subjected to ELISA to quantify circulatory PCSK9 levels. d Individual serum samples collected from group I, group II, group III, and group IV were subjected to ELISA to quantify murine PCSK9 levels. e PCSK9 transcripts in three representative tumor tissue samples from group III and group IV were analyzed by qRT-PCR. f Tumor or liver tissue lysates from three representative samples were resolved by SDS-PAGE and LDLR, and PCSK9 protein levels were analyzed by immunoblot. Band intensities were measured by densitometry and normalized with β-actin. The results are given as means ± standard deviation; *p < 0.05, **p < 0.01, ***p < 0.001 denote significant differences in the groups; ns non-significant