Published online May 7, 2014. doi: 10.3748/wjg.v20.i17.4953
Revised: December 4, 2013
Accepted: January 2, 2014
Published online: May 7, 2014
Processing time: 254 Days and 18.5 Hours
AIM: To clarify whether histone deacetylase inhibitors histone deacetylase inhibitors (HDACIs) can sensitize hepatocellular carcinoma (HCC) cells to sorafenib treatment.
METHODS: Bax, Bcl-2, ATG5-ATG12, p21, and p27 protein levels in Hep3B, HepG2, and PLC/PRF/5 cells were examined by Western blot. CCK8 and a fluorometric caspase-3 assay were used to examine cellular viability and apoptosis levels. The effect of Beclin-1 on sensitization of HCC cells to sorafenib was examined by transfecting Beclin-1 siRNA into Hep3B, HepG2, and PLC/PRF/5 cells.
RESULTS: Autophagy inhibition enhances the inhibitory effects of vorinostat and sorafenib alone or in combination on HCC cell growth. Vorinostat and sorafenib synergistically induced apoptosis and cell cycle alterations. Western blot data indicated that HDACIs and Beclin-1 knockdown increased the p53 acetylation level. The knockdown of Beclin-1 enhanced the synergistic effect of the combination of vorinostat with sorafenib.
CONCLUSION: HDACIs can sensitize HCC cells to sorafenib treatment by regulating the acetylation level of Beclin-1.
Core tip: In this study, we investigated the antiproliferative effect of sorafenib in combination with the histone deacetylase inhibitor vorinostatin in human hepatoma cell lines (Hep3B, HepG2, and PLC/PRF/5). We also examined whether the combination therapy was enhanced by the inhibition of autophagy. Our results showed that the combination of vorinostat with sorafenib synergistically reduced cell proliferation in hepatocellular carcinoma cells by inducing apoptosis and cell cycle arrest. Synergistic changes in cell cycle and cell survival regulators were also observed.