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The outcome of producing apoptotic defects in cancer cells is the primaryobstacle that limits the therapeutic efficacy of anticancer agents, and hencethe development of novel agents targeting novel non-canonical cell death pathwayshas become an imperative mission for clinical research. Fisetin (3,3',4',7-tetrahydroxyflavone)is a naturally occurring flavonoid commonly found in fruits and vegetables. Inthis study, we investigated the potential anticancer effects of fisetin on breastcancer cells. The result showed fisetin induced higher cytotoxicity in human breastcancer MCF-7 than in MDA-MB-231 cells otherwise it did not exert any detectablecytotoxicity in non-tumorigenic MCF-10A cells. We found fisetin can trigger anovel form of atypical apoptosis in caspase-3-deficient MCF-7 cells, which wascharacterized by several apoptotic features, including plasma membrane rupture,mitochondrial depolarization, activation of caspase-7, -8 and -9, and PARP cleavage;however, neither DNA fragmentation and phosphotidylserine (PS) externalizationwas observed. Although p53 was also activated by fisetin, the fisetin-inducedapoptosis was not rescued by the p53 inhibitor pifithrin-α. In contrast, the fisetin-inducedapoptosis was abrogated by pan-caspase inhibitor z-VAD-fmk. Furthermore, inhibitionof autophagy by fisetin was shown as additional route to prompt anticancer activityin MCF-7 cells. These data allow us to propose that fisetin appears as a new potentialanticancer agent which can be applied to develop a clinical protocol of humanbreast cancers.

international journal of oncology

Dietary flavonoid fisetin targets caspase-3-deficient human breast cancer MCF-7 cells by induction of caspase-7-associated apoptosis and inhibition of autophagy