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Carcinogenesis Advance Access originally published online on July 15, 2004
Carcinogenesis 2004 25(11):2183-2189; doi:10.1093/carcin/bgh233
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Carcinogenesis vol.25 no.11 © Oxford University Press 2004; all rights reserved.

ARTICLE

Curcumin induces c-jun N-terminal kinase-dependent apoptosis in HCT116 human colon cancer cells

Gavin P. Collett and Frederick Charles Campbell1

Department of Surgery, The Cancer Centre, Queen's University Belfast, Belfast BT12 6BJ, UK

1 To whom correspondence should be addressed Email: f.c.campbell{at}qub.ac.uk

Curcumin, the major pigment of the dietary spice turmeric has the potential for chemoprevention by promotion of apoptosis. Mitogen-activated protein kinase (MAPK) and NF-kappa B (NF{kappa}B) signalling cascades are thought to regulate apoptosis and cell survival. While curcumin inhibits NF{kappa}B, its effects upon the MAPK pathways are unclear. This study investigates curcumin effects upon MAPK signalling and apoptosis in HCT116 cells. Here we report that curcumin time- and dose-dependent induction of apoptosis were accompanied by sustained phosphorylation and activation of c-jun N-terminal kinase (JNK) and p38 MAPK as well as inhibition of constitutive NF{kappa}B transcriptional activity. Curcumin treatment also induced JNK-dependent sustained phosphorylation of c-jun and stimulation of AP-1 transcriptional activity. Curcumin-mediated c-jun phosphorylation and apoptosis were reduced by treatment with the JNK-specific inhibitor SP600125. Conversely, the p38-specific inhibitor SB203580 had no effect upon curcumin-induced apoptosis. Curcumin treatment had no effect on the activity of extracellular signal-regulated protein kinase (ERK). Taken together, our data show for the first time that JNK, but not p38 or ERK signalling, plays an important role in curcumin-mediated apoptosis in human colon cancer cells that may underlie its chemopreventive effects.


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