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. 2015 Jun 4;5:10893. doi: 10.1038/srep10893

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HDAB treatment activates the ATM-dependent DNA damage response and induces S phase arrest. An ATM kinase inhibitor, a CDK2 inhibitor and cyclin A2 siRNA can significantly increase the HDAB-induced apoptosis of cervical cancer cells. In addition, HDAB can function as an inhibitor of PARP to impair DNA repair, thereby enhancing cell death.