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Carcinogenesis Advance Access published online on February 23, 2006
Carcinogenesis, 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
Received August 3, 2005
Revised December 17, 2005
Accepted February 6, 2006

CARCINOGENESIS

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

Gavin P. Collett 1 and Frederick Charles Campbell 1 *

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

* To whom correspondence should be addressed.
Frederick Charles Campbell, E-mail: f.c.campbell{at}qub.ac.uk


  Abstract

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 antiapoptotic target genes including 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 MTT assay and 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 antiapoptotic 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 antiapoptotic genes.


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