FIGURE 7.

Increased GαS expression and acetylation are correlated with human hepatocarcinogenesis. (A) GαS, KAT7, and STAT3 phosphorylation were examined in human normal liver tissues and dysplastic nodule tissues from the indicated patients. (B) Acetylated GαS at K28 was examined in the precipitates using GαS antibody from human normal liver tissues and dysplastic nodule tissues as in (A). (C) Quantified levels of GαS, KAT7, STAT3 phosphorylation, and GαS acetylation in human normal liver tissues and dysplastic nodule tissues are shown (n = 12, unpaired t test). (D) The correlation between GαS and STAT3 phosphorylation in human dysplastic nodule tissues was analyzed by Pearson’s correlation coefficient assay (n = 12). (E) The correlation between acetylated GαS at K28 and STAT3 phosphorylation in human dysplastic nodule tissues was analyzed by Pearson’s correlation coefficient assay (n = 12). (F) Working model for KAT7‐acetylated and cytoplasm‐translocated GαS feedforward promoting the response to IL‐6 in liver cancer progenitors and driving hepatocarcinogenesis. Data are shown as mean ± SD, dot plots, or photographs directly as indicated. Abbreviations: DN, dysplastic nodule; IB, immunoblotting; IP, immunoprecipitation; N, normal; p‐, phosphorylated