Chidamide Combined With Doxorubicin Induced p53-Driven Cell Cycle Arrest and Cell Apoptosis Reverse Multidrug Resistance of Breast Cancer

The multidrug-resistant (MDR) phenotype is usually accompanied by an abnormal expression of histone deacetylase (HDAC). Given that HDAC vital in chromatin remodeling and epigenetics, inhibiting the role has become important approach for tumor treatment. However, effect inhibitors on MDR breast cancer not been elucidated. This study aim to demonstrate potential chidamide (CHI) combined with chemotherapy drug doxorubicin (DOX) overcome chemotherapeutic resistance vitro vivo , laying experimental foundation next clinical application. results showed that, CHI DOX significant cytotoxicity cells compared monotherapy. cell cycle distribution caused G0/G1 arrest inhibited growth regardless addition DOX. At same time, annexin V staining TUNEL enhanced number apoptosis drug-resistant cells. western blot analysis found p53 was activated CHI-treated group treatment group, then up-regulated p21, regulator recombinant protein (Puma), pro-apoptotic Bax, down-regulated apoptotic proteins Bcl-xL Bcl-2, caspase cascade induce apoptosis.