J. Cancer Mol.
4: 11-16, 2008
[Review Article]
Curcumin: a Potential Cancer Chemopreventive Agent
through Suppressing NF-kB
Signaling
Chih-Li
Lin and Jen-Kun Lin
Institute of Biochemistry and Molecular Biology, College
of Medicine, National Taiwan University, Taipei, Taiwan
Abstract:
Curcumin, a naturally occurring compound derived from turmeric, has long
been suggested with strong therapeutic or preventive potential to
against several major human diseases because of its anti-oxidative,
anti-inflammatory, and anti-cancerous effects. Although inflammation is
a protective effect, persistent inflammation has been believed to
involve in the multistage of cancer development. As a result, the
aberrantly increased activity of NF-kB, a master factor playing a key
role in inflammation, is implicated in a variety of human cancers.
Curcumin is known to exert anti-inflammatory effects significantly by
interrupting NF-kB signaling at multiple levels. Many observations
indicate that curcumin indeed shows valuable potential in the cancer
treatment through inhibiting the activity of I-kB kinase, IKK. In this
review, the anticancer effects of curcumin and the underlying mechanisms
are discussed. We also provide a summary of the recent literatures
focusing on NF-kB signaling pathways and their potential involvement in
the development of anticancer strategies.
(Keywords:
curcumin; NF-kB;
I-kB;
cancer prevention; inflammation)
_________________________________________________________________________________________________
Received 1/27/08; Revised 2/10/08; Accepted 2/12/08.
1. Correspondence:
Prof. Jen-Kun Lin, Institute of Biochemistry and Molecular Biology,
National Taiwan University College of Medicine, Room 947, No.
1, Jen-Ai Road Section 1, Taipei 100, Taiwan. Phone: 886-2-23123456 ext.
2213. Fax: 886-2-23918944. E-mail:
jklin@ha.mc.ntu.edu.tw
2. Abbreviations:
NF-kB,
nuclear factor kappa B; I-kB,
inhibitor of NF-kB;
IKK, I-kB
kinase; ROS, reactive oxygen species; MMP, matrix metalloproteinase;
TRAIL, TNF-related apoptosis inducing ligand; MAPK, mitogen-activated
protein kinase; COX-2, cyclooxygenase-2; ERK, extracellular
signal-regulated kinase.
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