8‑bromo‑7‑methoxychrysin induces apoptosis by regulating Akt/FOXO3a pathway in cisplatin‑sensitive and resistant ovarian cancer cells.

8‑bromo‑7‑methoxychrysin (BrMC), a novel chrysin analog, was reported to have anti‑cancer activities. The aim of the present study was to investigate the molecular mechanism of 8‑bromo‑7‑methoxychrysin (BrMC)‑induced apoptosis via the Akt/forkhead box O3a (FOXO3a) pathway in cisplatin (DDP)‑sensitive and ‑resistant ovarian cancer cells. The human ovarian cancer cell lines A2780 and A2780/DDP were cultured in vitro. Various molecular techniques were used to assess the expression of FOXO3a and B cell lymphoma 2 (Bcl‑2)‑interacting mediator of cell death (Bim) in cisplatin‑sensitive and ‑resistant ovarian cancer cells. Different concentrations of BrMC induced apoptosis in cisplatin‑sensitive and ‑resistant ovarian cancer cells. BrMC‑induced apoptotic cell death occurred mainly by the activation of Akt, which was accompanied by the overexpression of transcription factor FOXO3a, with a concomitant increase in the expression levels of Bim. Silencing Bim expression by using small interfering RNA, attenuated the induction of apoptosis by BrMC treatment. The results indicated that BrMC‑induced apoptosis in cisplatin‑sensitive and ‑resistant ovarian cancer cells may occur via the regulation of Akt/FOXO3a, leading to Bim transcription.