Objective We attempted to survey the inhibit effect of fisetin with human ovarian cancer cell line SKOV3 and the xenograft and the mechanism of the effect. Methods The ovarian cancer cell line SKOV3 treated by fisetin were observed directly under the transmission electronmicroscope (TEM); MTT assay was used to determine cell viability. Flow cytometry was used to analyze the apoptosis in ovarian cancer cell line SKOV3. In addition, we established an ovarian cancer athymicnude rat model. We observed the neoplasia and progression after fisetin treatment. The proliferation and apoptosis of athymic nude rat model were evaluated by testing Bcl-2, Bax and poly-ADP-ribose polyerase (PARP) expression through Western blot. Results The chromatin were brought together and the apoptotic bodies were detected in SKOV3 cells under transmission electron microscope after the treatment by fisetin. MTT assay indicated that fisetin inhibited ovarian cancer cell proliferation in a dose-dependent manner. The flow cytometry data demonstrated that the apoptosis might induct in SKOV3 cells after treatment by fisetin. In athymic rude rat model, under the influence of fisetin, tumor volume and tumor mass were significantly decreased. Western blot demonstrated that treatment with higher concentration of fisetin resulted in a significant decrease of Bcl-2 and a significant increase of Bax. The apoptosis proteins PARP was cut apparently. Conclusion The results provided the first insight into antitumor anti-proliferative and the induction of apoptosis efficacy of fisetin against ovarian cancer in vitro and in vivo. All data suggested a safe promising therapeutic potential of fisetin in ovarian cancer treatment.
