Pharmacological inhibition of HDAC1/3-interacting proteins induced morphological changes, and hindered the cell proliferation and migration of hepatocellular carcinoma cells.

Liver diseases are particularly severe health problems, but the options available for preventing and treating them remain limited. Accumulating evidence has shown that there is altered expression of individual histone deacetylase (HDAC) family members in hepatocellular carcinoma cells. In a previous study, we have identified a set of proteins which interact with histone deacetylase 1 and 3 (HDAC1/3) in hepatocellular carcinoma cell lines HepG2 by proteomic approach. This study was designed to investigate the therapeutic potential and expression of HDAC1/3-interacting genes in a human hepatocellular carcinoma cell line (HepG2). Pharmacological and transcriptional inhibition of HDAC1/3 resulted in the suppression of cancer cell proliferation, change of cell morphology, and downregulation of HDAC1/3 genes in HepG2 cells. The pharmacological inhibition also resulted in inhibition of liver cancer cell migration by wound scratch assay. Taken together, the results from this study show that the upregulation of HDAC1/3 in hepatocellular carcinoma resulted in the overexpression of CNOT1, PFDN2/6, and HMG20B, and that these genes could serve as novel molecular targets in liver cancer.

The Protective Properties of the Strawberry (Fragaria ananassa) against Carbon Tetrachloride-Induced Hepatotoxicity in Rats Mediated by Anti-Apoptotic and Upregulation of Antioxidant Genes Expression Effects.

The strawberry (Fragaria ananassa) has been extensively used to treat a wide range of ailments in many cultures. The present study was aimed at evaluating the hepatoprotective effect of strawberry juice on experimentally induced liver injury in rats. To this end, rats were introperitoneally injected with carbon tetrachloride (CCl4) with or without strawberry juice supplementation for 12 weeks and the hepatoprotective effect of strawberry was assessed by measuring serum liver enzyme markers, hepatic tissue redox status and apoptotic markers with various techniques including biochemistry, ELISA, quantitative PCR assays and histochemistry. The hepatoprotective effect of the strawberry was evident by preventing CCl4-induced increase in liver enzymes levels. Determination of oxidative balance showed that strawberry treatment significantly blunted CCl4-induced increase in oxidative stress markers and decrease in enzymatic and non-enzymatic molecules in hepatic tissue. Furthermore, strawberry supplementation enhanced the anti-apoptotic protein, Bcl-2, and restrained the pro-apoptotic proteins Bax and caspase-3 with a marked reduction in collagen areas in hepatic tissue. These findings demonstrated that strawberry (F. ananassa) juice possessed antioxidant, anti-apoptotic and anti-fibrotic properties, probably mediated by the presence of polyphenols and flavonoids compounds.