HDAC1 and hepatocellular carcinoma: Figure 4 shows that after exposing drug-resistant HCC Bel7402/5-FU cells to vehicle, CHC (2.0 and 5.0 μM), and SAHA (5.0 μM) for 72 h, CHC promoted the acetylation of H3, H4, and α-tubulin with increasing dose, which coincided with the observed high HDAC1 and HDAC6 enzyme activities.