TY - JOUR
T1 - Inflexinol inhibits colon cancer cell growth through inhibition of nuclear factor-κB activity via direct interaction with p50
AU - Jung, Ok Ban
AU - Ju, Hoon Oh
AU - Bang, Yeon Hwang
AU - Dong, Cheul Moon
AU - Jeong, Heon Sang
AU - Lee, Seram
AU - Kim, Soyoun
AU - Lee, Hyosung
AU - Kim, Kyung Bo
AU - Sang, Bae Han
AU - Jin, Tae Hong
PY - 2009/6
Y1 - 2009/6
N2 - Kaurane diterpene compounds have been known to be cytotoxic against several cancer cells through inhibition of nuclear factor-κB (NF-κB) activity. Here, we showed that inflexinol, a novel kaurane diterpene compound, inhibited the activity of NF-κB and its target gene expression as well as cancer cell growth through induction of apoptotic cell death in vitro and in vivo. These inhibitory effects on NF-κB activity and on cancer cell growth were suppressed by the reducing agents DTT and glutathione and were abrogated in the cells transfected with mutant p50 (C62S). Sol-gel biochip and surface plasmon resonance analysis showed that inflexinol binds to the p50 subunit of NF-κB. These results suggest that inflexinol inhibits colon cancer cell growth via induction of apoptotic cell death through inactivation of NF-κB by a direct modification of cysteine residue in the p50 subunit of NF-κB.
AB - Kaurane diterpene compounds have been known to be cytotoxic against several cancer cells through inhibition of nuclear factor-κB (NF-κB) activity. Here, we showed that inflexinol, a novel kaurane diterpene compound, inhibited the activity of NF-κB and its target gene expression as well as cancer cell growth through induction of apoptotic cell death in vitro and in vivo. These inhibitory effects on NF-κB activity and on cancer cell growth were suppressed by the reducing agents DTT and glutathione and were abrogated in the cells transfected with mutant p50 (C62S). Sol-gel biochip and surface plasmon resonance analysis showed that inflexinol binds to the p50 subunit of NF-κB. These results suggest that inflexinol inhibits colon cancer cell growth via induction of apoptotic cell death through inactivation of NF-κB by a direct modification of cysteine residue in the p50 subunit of NF-κB.
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U2 - 10.1158/1535-7163.MCT-08-0694
DO - 10.1158/1535-7163.MCT-08-0694
M3 - Article
C2 - 19509257
AN - SCOPUS:67649360284
SN - 1535-7163
VL - 8
SP - 1613
EP - 1624
JO - Molecular Cancer Therapeutics
JF - Molecular Cancer Therapeutics
IS - 6
ER -