Journal
MOLECULES
Volume 23, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/molecules23051095
Keywords
kaempferol; cell cycle arrest; Chk2; apoptosis; DR5; Fas
Funding
- NIH from the National Center for Research Resources [P20RR016477]
- National Institute for General Medical Sciences (NIGMS) [P20GM103434]
- NIGMS, a component of the National Institutes of Health (NIH) [P20GM104932]
- COBRE [GM102488/RR032138]
- ARIA S10 [RR020866]
- FORTESSA S10 [OD016165]
- INBRE [GM103434]
- China Postdoctoral Science Foundation [2017M611065]
- Zhejiang Province Postdoctoral Science Grant
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Kaempferol is a widely distributed dietary flavonoid. Epidemiological studies have demonstrated kaempferol consumption lowers the risk of ovarian cancer. Our previous research proved that kaempferol suppresses human ovarian cancer cells by inhibiting tumor angiogenesis. However, the effects of kaempferol on the cell cycle and extrinsic apoptosis of ovarian cancer cells have not yet been studied. In the present study, we demonstrated that kaempferol induced G2/M cell cycle arrest via the Chk2/Cdc25C/Cdc2 pathway and Chk2/p21/Cdc2 pathway in human ovarian cancer A2780/CP70 cells. Chk2 was not responsible for kaempferol-induced apoptosis and up-regulation of p53. Kaempferol stimulated extrinsic apoptosis via death receptors/FADD/Caspase-8 pathway. Our study suggested that Chk2 and death receptors played important roles in the anticancer activity of kaempferol in A2780/CP70 cells. These findings provide more evidence of the anti-ovarian cancer properties of kaempferol and suggest that kaempferol could be a potential candidate for ovarian cancer adjuvant therapy.
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