The apoptosis machinery is compromised in liver cancer (LC). The underlying mechanism needs to be further investigated. Histone deacetylases (HDAC) have multiple and strong biochemical activities. This study tests a hypothesis that HDAC11 prevents LC cell (LCC) apoptosis via modulating the p53 gene transcription. In this study, the LC tissues were collected from patients with LC. The LCCs were purified by magnetic cell sorting. The gene transcription activities of the LCCs were analyzed by immunoprecipitation (IP) and chromatin IP. We observed that the LCCs expressed high levels of HDAC11, which was negatively correlated with the expression of p53 in LCCs. Further findings indicated that HDAC11 formed a complex with Egr1, the transcription factor of p53. HDAC11 induced Egr1 deacetylation and thus prevented the p53 gene transcription. Over expression of HDAC11 in liver cells inhibited the cell apoptosis. Inhibition of the expression of HDAC11 in LCCs promoted the LCC apoptosis. In conclusion, HDAC11 plays a critical role in the compromising the expression p53 in LCC, which can be reversed by the inhibition of HDAC11. To regulate HDAC11 may have therapeutic potential for LC treatment.
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