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Carcinogenesis Advance Access originally published online on February 23, 2006
Carcinogenesis 2006 27(6):1285-1291; doi:10.1093/carcin/bgi368
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Overexpression of p65/RelA potentiates curcumin-induced apoptosis in HCT116 human colon cancer cells

Gavin P. Collett and Frederick C. Campbell *

Department of Surgery, Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT12 6BJ, UK

* To whom correspondence should be addressed. Tel: +44 2890 322276; Fax: +44 2890 321811; Email: f.c.campbell{at}qub.ac.uk

Curcumin, the yellow pigment in the spice turmeric, has potent chemopreventive activities that involve diverse molecular pathways. It is widely believed that curcumin pro-apoptotic properties are mediated by downregulation of NF kappa B (NF{kappa}B). The p65/RelA subunit of NF{kappa}B may influence cell death, in part by activation of NF{kappa}B anti-apoptotic target genes including X-linked inhibitor of apoptosis (XIAP), A20, bcl-xL and inhibition of sustained activation of c-Jun N-terminal kinase (JNK). We have shown previously that curcumin inhibits NF{kappa}B, activates JNK and promotes apoptosis in HCT116 colorectal cancer cells. Here, we show that forced overexpression of p65 does not affect curcumin-induced JNK activation. Indeed, overexpression of p65 enhanced curcumin-mediated apoptosis as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay and poly(ADP-ribose) polymerase (PARP) cleavage. This potentiating effect of p65 upon curcumin-mediated apoptosis was reversed by transfection of cells with an I{kappa}B super-repressor ({Delta}NI{kappa}B). Curcumin treatment inhibited expression of NF{kappa}B anti-apoptotic target genes in mock-transfected and in p65-overexpressing HCT116 cells, although expression levels remained higher in the latter. Taken together, these results show that curcumin-mediated activation of JNK or induction of apoptosis does not require inhibition of p65. Furthermore, curcumin/p65 synergy in promotion of apoptosis cannot be attributed to active repression of NF{kappa}B anti-apoptotic genes.


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