Effect of fisetin on the proliferation and migration of human breast and cervical cancer cells

Purpose: To explore the fisetin effects on the growth, apoptosis, and migration in human breast and cervical cancer cells, MCF-7 and HeLa cells, respectively. Methods: Cell cycle arrest was used for the determination of cell growth and sulforhodamine B (SRB) colony formation. Gene expression was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), while cell migration was assessed by wound healing and matrigel migration assays. Results: The data indicate that fisetin activated breast and cervical cancer cell death, and this was confirmed by decreased cell growth, changed cell morphology, and arrested cell cycle at G2/M phase. During the incubation period, fisetin inhibited cancer cells at low concentration with half-maximal concentration (IC50) values of 267.10 +/- 48.96, 88.42 +/- 1.35 and 41.03 +/- 8.04 mu g/mL after 24, 48 and 72 h, respectively, for MCF-7 cells; and 140.97 +/- 22.92, 100.84 +/- 10.97 and 95.53 +/- 14.33 mu g/mL, respectively, for HeLa cells (p < 0.05). Fisetin suppressed the migration of the cancer cells by inhibiting wound healing and suppressing cell migration to the lower chamber. Moreover, fisetin inhibited cancer cells growth by reducing the gene expression of cyclin D1 and cyclin E. Conclusion: Fisetin reduces cancer cell death, activates apoptosis and suppresses cancer cell migration. Therefore, fisetin is a potential anticancer agent for the prevention and treatment of breast and cervical cancers in humans, but further development studies are required in this regard.

Automated summary

Fisetin exerts inhibitory effects on human breast and cervical cancer cells, reducing cell growth, activating apoptosis, and suppressing cell migration. The results suggest that fisetin may be a potential anticancer agent for the treatment of breast and cervical cancers in humans.