Fig. 4: The HDAC3 deficiency suppresses hepatocyte proliferation and STAT3 signaling in vitro. | Cell Death & Disease

Fig. 4: The HDAC3 deficiency suppresses hepatocyte proliferation and STAT3 signaling in vitro.

From: Histone deacetylase 3 promotes liver regeneration and liver cancer cells proliferation through signal transducer and activator of transcription 3 signaling pathway

Fig. 4

a Living hepatocyte numbers show that cell number of the mutant diploid hepatocyte is continuously decreased. The values are normalized to the average cell numbers on 0 h. b The cell cycle of in vitro diploid hepatocytes following mitogen stimulation for 48 h was determined by flow cytometry analysis. c Cell growth in HepG2 cells was tested after HDAC3 knockdown using a CCK-8 kit. d Western blot analysis demonstrates that STAT3(Y705) fails to be phosphorylated due to the high level of ac-STAT3 in the primary mutant hepatocytes after the IL6 treatment. β-Actin and histone H3 were used as the loading controls. e Immunofluorescence shows that STAT3 is unable to accumulate in the nuclei of the mutant hepatocytes following IL6 stimulation for 30 min (scale bar: 5 μm). f Immunofluorescence demonstrates that p-STAT3(Y705) remains absent in the mutant hepatocytes after the IL6 treatment (scale bar: 5 μm). All data represent the mean ± SD; n = 3–5; *p < 0.05; **p < 0.01; ***p < 0.001

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