Premium
Effect of the dietary compound fisetin on nuclear factor‐kappa B (NF‐κB) signaling in HT‐29 colon cancer cells
Author(s) -
Seon Mi Ra,
Cho Han Jin,
Kang IlJun,
Kim HyeMi,
Jeung SeungKyoung,
Park Jung HY
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a360-a
Subject(s) - fisetin , western blot , nf κb , chemistry , downregulation and upregulation , apoptosis , kinase , signal transduction , iκb kinase , cell growth , nfkb1 , microbiology and biotechnology , biochemistry , biology , flavonoid , antioxidant , transcription factor , gene
Flavonoids have been reported to have ability to prevent cancer development. Fisetin, a naturally occurring flavonol, is commonly found in fruits, vegetables, and wine. We have previously observed that fisetin inhibits HT‐29 human colon cancer cell growth. To examine the effect of fisetin on the NF‐κB signaling that is known to play an important role in cell survival and apoptosis, HT‐29 cells were treated with 0 or 60 μmol/L fisetin for 10 min, 30 min or 120 min. Western blot analysis revealed that fisetin increased p‐IκB α protein levels at 10 and 30 min of culture, and decreased IκB α protein levels after 30 min treatment. Immunoprecipitation and in vitro kinase assay revealed that fisetin dose‐dependently increased IκB kinase (IKK) activity. The subcellular fractionation and immunocytochemistry assay revealed that fisetin increased translocation of p65 (RelA) to the nucleus. In addition, electrophoretic mobility shift assay indicated that fisetin increased NF‐κB DNA binding activity in a concentration‐dependent manner. These results raised the possibility that fisetin may inhibit HT‐29 cell growth via its ability to upregulate NF‐κB signaling.