Figure 6: ACSS1/2 positively correlates with histone acetylation and FASN expression in human hepatocellular carcinoma.
From: Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
(a) FASN, ACSS1 and ACSS2 protein levels (upper panels, normalized against β-actin) and H3K9, H3K14, H3K18, H3K23, H3K27 and H3K56 acetylation levels (lower panels, normalized against histone H3) in 53 pairs of HCC (each paired with cancerous tissue (designated as C) and adjacent normal tissue (designated as N)) were analysed by western blot. Two pairs of representative samples were shown. For the other 51 pairs of samples, please refer to Supplementary Fig. 6b. (b) Heatmap of protein expression (ACSS1, ACSS2 and FASN) and histone acetylation levels (H3K9ac, H3K14ac, H3K18ac, H3K23ac, H3K27ac and H3K56ac) in all 53 pairs of HCC. Data were presented as Z-score of relative protein expression or histone acetylation. Tumours with 1.5-fold higher expression of ACSS1 or ACSS2 or both than that of adjacent normal control tissue are grouped into ACSS-high tumours (tumour/normal ≥1.5, n=26), while ACSS-low tumours (tumor/normal<1.5, n=27) express both ACSS proteins at 1.5-fold lower than its normal control. (c) H3K9ac (P=0.0220), H3K14ac (P=0.0289), H3K27ac (P=0.0034), and H3K56ac (P=0.0410), are significantly stronger in ACSS-high tumours than that in ACSS-low tumours. Statistical analyses were performed with a two-tailed unpaired Student’s t-test (*P<0.05; **P<0.01; NS, not significant). (d) FASN protein level is significantly upregulated in ACSS-high tumours (P=0.002). Statistical analyses were performed with a two-tailed unpaired Student’s t-test (**P<0.01). (e) Representative immunohistochemical staining results for ACSS1, ACSS2, FASN and H3K9/K27/K56 acetylation in adjacent normal tissue (N) and hepatocellular carcinoma (C). Scale bar, 100 μm.
