Fig. 5.

HNF4A and HIC1 have the opposite function to affect liver tumorigenesis. (A) Overexpression of HNF4A and HIC1 had the opposite function in regulating liver tumorigenesis. Mice were injected with pLIVE liver-specific expressing plasmids that overexpressing HNF4A-Myc or HIC1-FLAG via the tail vein prior to the treatment of DEN/CCl4. Livers from mice under the indicated treatment are shown (n = 5/group). c-PARP, HMGB1, GPX4, HBA1 and STMN1 from the liver, as indicated, were measured by IHC. Scale bar, 200 μm. (B) Knocking out HIC1 and HNF4A led to opposite outcomes in liver tumorigenesis. Livers from WT, HIC1−/− and HNF4A−/− mice are shown (n = 5/group). The indicated proteins in the liver were measured by IHC. Scale bar, 200 μm. (C) Colony formation capacities in the hepatocyte line (HL-7702 and THLE-3) and liver cancer cell line (HepG2 and Bel-7402) under indicated treatment, as measured by the soft agar colony formation assay. Scale bar, 200 μm. (D) Volume of xenograft formed by the Bel-7402 cells was graphed (left, n = 5/group). WB of HNF4A, HIC1, GPX4, HBA1 and STMN1 in the xenograft are also shown (right). **, p < 0.01 indicate statistical significance. The data were analyzed by a one-way ANOVA test (Fig. 5D). Images of IHC, colony formation, and WB are representative ones of 3 independent experiments.