Fisetin induces apoptosis in human nonsmall lung cancer cells via a mitochondria-mediated pathway.

Abstract

The present study investigated the apoptotic effects of fisetin, a phenolic compound, against the human nonsmall cell lung cancer cell line, NCI-H460. Fisetin showed dose-dependent cytotoxic activity against NCI-H460 cells, with 50% inhibition of cell viability occurring at a concentration of 75 μg/mL. Fisetin induced both the production of intracellular reactive oxygen species and apoptosis, as evidenced by apoptotic body formation, DNA fragmentation, an increase in the number of sub-G1 phase cells, and mitochondrial membrane depolarization. Moreover, fisetin significantly modulated the expression of apoptosis-associated proteins, resulting in reduced expression of B cell lymphoma-2, increased expression of Bcl-2-associated X protein, and activation of caspase-9 and caspase-3. In addition, pretreatment with a caspase inhibitor blocked fisetin-induced cell death.

• Authors: Kyoung Ah Kang, Mei Jing Piao, Jin Won Hyun
• Journal: In vitro cellular & developmental biology. Animal (In Vitro Cell Dev Biol Anim) Vol. 51 Issue 3 Pg. 300-9 (Mar 2015) ISSN: 1543-706X [Electronic] Germany
• PMID: 25381036 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Flavonoids
• Flavonols
• Reactive Oxygen Species
• Caspases
• fisetin

Topics

• Apoptosis (drug effects)
• Carcinoma, Non-Small-Cell Lung (enzymology, pathology)
• Caspases (metabolism)
• Cell Line, Tumor
• Cell Survival (drug effects)
• Flavonoids (pharmacology)
• Flavonols
• Humans
• Intracellular Space (metabolism)
• Lung Neoplasms (enzymology, pathology)
• Mitochondria (drug effects, metabolism)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (drug effects)