Anti-proliferative effect and cell cycle arrest induced by saponins extracted from tea (Camellia sinensis) flower in human ovarian cancer cells

- Reported for the first time the anti-cancer effect of TFS against ovarian cancer.
- TFS inhibited the growth of ovarian cancer cells at low concentrations.
- TFS induced p53-dependent apoptosis and two apoptotic pathways were activated.
- S phase arrest induced by TFS was via Cdc25A-Chk2-CyclinE/A pathway.
- Chk2-Cdc25A DNA damage response pathway was activated in the S phase arrest.

Tea (Camellia sinensis) flower saponins (TFS) have various biological properties. However, the anti-cancer effects of TFS have not been investigated in any detail. Here, we evaluated the anti-cancer effects of TFS using human ovarian cancer cell lines. TFS (1.5 μg/ml) produced significant antiproliferative effects against A2780/CP70 and OVCAR-3 cells by inducing p53-dependent apoptosis and S phase arrest. Further study showed that TFS decreased mitochondrial membrane potential, activated Caspase-3/7, Caspase-8 and Caspase-9 activities, and that the p53 inhibitor PFT-α reversed the TFS-induced cell growth inhibition and apoptosis. In addition, TFS inhibited the expression of Cdc25A, Cdk2, and CyclinD1 and upregulated Cyclin E and Cyclin A, suggesting that the Cdc25A-Cdk2-Cyclin E/A pathway was involved in TFS-induced S phase arrest. Furthermore, the S phase arrest was associated with a Chk2-Cdc25A DNA damage response. These results demonstrated that TFS has promising potential serving as functional food components for prevention of ovarian cancer.