Daidzein induces choriocarcinoma cell apoptosis in a dose-dependent manner via the mitochondrial apoptotic pathway.

Abstract

Choriocarcinoma is a malignant gestational trophoblastic disease and relapse or drug resistance occurs in ~25% of gestational trophoblastic tumors. Cell apoptosis serves a role in the progression from hydatidiform mole to persistent gestational trophoblastic disease. It has been demonstrated that daidzein [7‑hydroxy‑3‑(4‑hydroxyphenyl)‑4H‑chromen‑4‑one] may induce apoptosis in a number of cancer types via the mitochondrial apoptotic pathway by altering the B‑cell lymphoma (Bcl)‑2/Bcl‑2 associated X, apoptosis regulator (Bax) ratio, and activating the caspase cascade. Daidzein also serves a role in regulation of production of human chorionic gonadotropin in trophoblast cells and inhibition of cell proliferation. However, few reports have been published regarding the effect of daidzein on apoptosis in choriocarcinoma. Therefore, in the present study, JAR and JEG‑3 human gestational choriocarcinoma cells were used to investigate the effect of daidzein on apoptosis of choriocarcinoma cells. Treatment with daidzein for 48h reduced cell viability in a dose‑dependent manner. The percentages of early and late apoptotic cells also increased following treatment with daidzein in a dose‑dependent manner, with the number of late apoptotic cells increasing more prominently. Furthermore, treatment with daidzein led to apoptosis‑associated alterations in nuclear morphology of JAR and JEG-3 cells. Expression levels of cleaved poly(ADP‑ribose) polymerase, cleaved caspase‑3 and cleaved caspase‑9 increased following treatment with daidzein, whereas the Bcl‑2/Bax ratio decreased in a dose‑dependent manner. In conclusion, the results of the present study demonstrate that daidzein may induce apoptosis of choriocarcinoma cells in a dose‑dependent manner via the mitochondrial apoptotic pathway.