Fisetin (3,7,3′,4′‐tetrahydroxyflavone), a bioactive dietary flavonoid, intrigued scientists for its anticancer potential against various cancer types. We investigated the fisetin‐induced inhibition of growth and survival of human hepatocellul...
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https://www.riss.kr/link?id=O112636558
2020년
-
0951-6433
1872-8081
SCIE;SCOPUS
학술저널
118-135 [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
Fisetin (3,7,3′,4′‐tetrahydroxyflavone), a bioactive dietary flavonoid, intrigued scientists for its anticancer potential against various cancer types. We investigated the fisetin‐induced inhibition of growth and survival of human hepatocellul...
Fisetin (3,7,3′,4′‐tetrahydroxyflavone), a bioactive dietary flavonoid, intrigued scientists for its anticancer potential against various cancer types. We investigated the fisetin‐induced inhibition of growth and survival of human hepatocellular carcinoma. Fisetin decreased cell viability and proliferation of HepG2 cells as revealed from MTT and clonogenicity assays. Cell cycle arrest in the G2/M phase was observed. Annexin V/propidium iodide (PI) staining followed by flow cytometry revealed that fisetin induced both apoptosis and necroptosis in HepG2 cells. Apoptotic cells were significantly increased on fisetin treatment as observed in morphological evaluations and 4′,6‐diamidino‐2‐phenylindole and Acridine orange staining. Flow cytometry, fluorescence imaging, and 2′, 7′‐dichlorofluorescein diacetate analyses showed an increase in reactive oxygen species (ROS) generation on fisetin treatment. Pretreatment with N‐acetyl cysteine inhibited ROS production and also rescued mitochondrial membrane potential in HepG2 cells. The underlying mechanisms of apoptosis and necroptosis were determined by analysis of their respective signaling molecules using qRT‐PCR and Western blotting. Fisetin showed a marked increase in the expression of TNFα and IKκB with a decrease in NF‐κB, pNF‐κB and pIKκB expression. Fisetin reduced the expression of Bcl2, and elevated levels of Bax, caspase‐3, and PARP and thus induced apoptosis in HepG2 cells. zVAD suppressed the fisetin‐induced expression of caspase‐8, RIPK1, RIPK3, and MLKL as opposed to fisetin treatment. Nec‐1 + fisetin could not completely block necroptosis, which warrants further investigation. Taken together, our findings demonstrate that the fisetin exhibited anti‐proliferative effects on HepG2 cells through apoptosis and necroptosis via multiple signaling pathways. Fiestin has potential as a therapeutic agent against hepatocellular carcinoma.
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