Fig. 3: Schematic diagram to identify differentially expressed proteins resulting from the stat4 polymorphism: possible regulation of the CYP2E1/FGL2 pathway.
A An enrichment analysis of the KEGG pathway for differentially expressed proteins in hepatofibrotic tissue of HCC patients. B Venn diagram showing the number of differential proteins in hepatofibrotic tissue of HCC patients. C Functional classification of differentially expressed proteins affected by the STAT4 expression and HCC: inflammation, angiogenesis, proliferation, immunity, and metabolism. Inflammation: MVP Major vault protein, STAT1 Signal transducer and activator of transcription 1. Angiogenesis: PFN Profilin-1, MME Neprilysin, NPNT Nephronectin. Proliferation: INHBE Inhibin beta E chain, BBOX1 Gamma-butyrobetaine hydroxylase1. Immunity: LGALS9 Galectin-9, FGL2 Fibroleukin (Fibrinogen-like protein 2), TAPBP Tapasin (TAP-binding protein); PARP4-Poly [ADP-ribose] polymerase 4; ELMO2 Engulfment and cell motility protein 2. Metabolism: BCAT2 Branched-chain amino acid aminotransferase, DHRS2 Dehydrogenase/reductase SDR family member 2; GYS2 Glycogen synthase, G6PD Glucose-6-phosphate 1-dehydrogenase, RBP4 Retinol binding protein 4, BCHE Choline-esterase. D Kaplan–Meier curve of overall survival for patients grouped by median of FGL2 expression levels, P-values are depicted by Cox–Mantel log-rank test. E, F The correlation between the expression of FGL2 and the activity of CYP2E1 (Vmax and Clint) in human HCC liver tissue, R and P-values by Pearson’s correlation test are depicted. G The expression of FGL2 on the median of Vmax and Clint as the cutoff point, in HCC liver tissue by Western blot. GAPDH in each lane served as an internal control for normalization (N = 3), *P < 0.05 was assessed by Student’s t-test.
