FIGURE 2.

GαS‐promoted hepatocarcinogenesis is dependent on IL‐6. (A) Tumor incidence (chi‐squared test), number, and maximum diameter (unpaired t test) of DEN‐induced HCC in male GαS^F/F(OVER) , GαS^hep+/+ , Il6^−/− , and GαS^hep+/+Il6^−/− mice were analyzed (n = 12). (B) Tumor incidence (chi‐squared test), number, and maximum diameter (unpaired t test) of DEN‐induced HCC in male GαS^F/F(OVER)Il6ra^F/F , GαS^hep+/+ , Il6ra^hep−/− , and GαS^hep+/+Il6ra^hep−/− mice were analyzed (n = 12). (C) Nonaggregated hepatocytes and isolated HcPCs were stimulated with IL‐6 for the indicated time periods, and STAT3 phosphorylation was examined. (D) Isolated HcPCs from male GαS^F/F(OVER) and GαS^hep+/+ mice were stimulated with IL‐6 for the indicated time periods, and STAT3 phosphorylation was examined. (E) Isolated HcPCs from male GαS^F/F(KO) and GαS^hep−/− mice were stimulated with IL‐6 for the indicated time periods, and STAT3 phosphorylation was examined. (F) Tumor number and maximum diameter were analyzed in male mice transplanted by intrasplenic injection with isolated HcPCs from male GαS^F/F(OVER) and GαS^hep+/+ mice (n = 6, unpaired t test). (G) Tumor number and maximum diameter were analyzed in male mice transplanted by intrasplenic injection with isolated HcPCs from male GαS^F/F(KO) and GαS^hep−/− mice (n = 6, unpaired t test). Data are shown as mean ± SD or photographs from one representative of three independent experiments. ^△ p > 0.05, *p < 0.05, **p < 0.01