Abstract

Endometrial cancer is a serious malignant disease in women and causes thousands of deaths each year. Due to the lack of effective drugs and/or therapies, patients with late-stage disease often have a poor prognosis. Erianin is a natural product that exerts an inhibitory effect on several types of cancer. In this study, erianin was shown to inhibit cell proliferation and cell invasion by inducing apoptosis in endometrial cancer cells in vitro . Erianin increased the levels of the Bcl-2 family apoptosis regulator BOK and activated caspase-3 but decreased Bcl-2 levels. Furthermore, knockdown of the BOK gene decreased cell apoptosis, suggesting that erianin might activate the caspase-3-mediated apoptosis pathway. Based on the TargetScan database, the potential binding site between BOK and miR-661 was detected. BOK mRNA levels were increased by the miR-661 inhibitor but decreased by the miR-661 mimics. Moreover, a luciferase reporter assay confirmed the interaction of miR-661 with BOK. Consistent with these findings, miR-661 mimics rescued the inhibitory effect of erianin on endometrial cancer cells. However, BOK overexpression relieved the effect of miR-661 mimics. In conclusion, erianin regulated tumorigenesis in endometrial cancer by enforcing BOK expression through the inhibition of miR-661. Graphical abstract