A new study has reported that the flavonoid fisetin can induce cell death in breast cancer cells without harming normal breast cells. The apoptotic effect was stronger in hormone receptor positive (ER+/PR+) than in hormone receptor negative (ER-/PR-) cells. Fisetin is a flavonol found in fruits and vegetables, most abundantly in strawberries and onions, but also in apples, persimmons, grapes, and cucumbers. Many anticancer treatments are designed to promote cancer cell death. Hence, the development of agents targeting new cell death pathways is important in clinical research. Fisetin has previously been shown to induce apoptosis (programmed cell death) in human colon and prostate cancer cells.

In the present study, fisetin was found to induce higher cytotoxicity in ER+/PR+ MCF-7 human breast cancer cells than in ER-/PR- MDA-MB-231 cells. However, fisetin was not found to cause cell death in non-cancerous breast cells. The authors found that fisetin can trigger a new form of atypical apoptosis in caspase-3-deficient MCF-7 cells (caspase-3 is an enzyme that plays an essential role in programmed cell death). Furthermore, fisetin inhibited autophagy. Autophagy is a type of cell self-digestion which can stop normal cells from developing into cancer cells and lead to cell death. However, autophagy can also protect cancer cells. Breast cancer cells use autophagy as a survival mechanism in response to nutrient starvation, exposure to DNA damaging agents, and tamoxifen treatment. Therefore, fisetin's inhibition of autophagy served as an additional route to anticancer activity in MCF-7 cells. The authors conclude that the study results indicate that fisetin may be a new potential anticancer agent for human breast cancer.

Please see our articles on what hormone receptor positive or hormone receptor negative breast cancer patients and survivors should eat for more information.