Fig. 2
From: JMJD4-demethylated RIG-I prevents hepatic steatosis and carcinogenesis
Decreased RIG-I in liver cancer progenitor HcPCs promotes their response to IL-6, which viciously drives their progression to established HCC. a STAT3 phosphorylation and activation were examined in liver tissues from male Rig-If/f and Rig-Ihep−/− mice 48 h post-DEN administration. b Tumor incidence (chi-square test), number and maximum diameter (unpaired t-test) of DEN-induced HCC in male Rig-If/fIL-6−/− and Rig-Ihep−/−IL-6−/− mice were analyzed (n = 12). c Tumor incidence (chi-square test), number and maximum diameter (unpaired t-test) of DEN-induced HCC in male IL-6rahep−/− and Rig-Ihep−/−IL-6rahep−/− mice were analyzed (n = 12). d IL-6-induced STAT3 phosphorylation in the indicated time periods was examined in liver tissues and isolated hepatocytes from male Rig-If/f and Rig-Ihep−/− mice. e IL-6-induced Saa1 mRNA expression in the indicated time periods was examined in liver tissues and isolated hepatocytes from male Rig-If/f and Rig-Ihep−/− mice (n = 4, unpaired t-test). f Isolated nonaggregated hepatocytes and HcPCs were stimulated with IL-6 for the indicated time periods, and STAT3 phosphorylation was examined. g Isolated nonaggregated hepatocytes and HcPCs from control AAV8 or AAV8-RIG-I-treated male mice were stimulated as in f, and STAT3 phosphorylation was examined. h Isolated HcPCs from male Rig-If/f and Rig-Ihep−/− mice were stimulated with IL-6 for 30 min, and STAT3 phosphorylation was examined. i Tumor number and maximum diameter were analyzed in male mice transplanted by intrasplenic injection with equal amounts of isolated HcPCs from Rig-If/f and Rig-Ihep−/− mice (n = 6, unpaired t-test). Data are shown as mean ± s.d. or photographs from one representative of three independent experiments. *P < 0.05, **P < 0.01, ▲P > 0.05