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Review
. 2009 Sep;11(3):495-510.
doi: 10.1208/s12248-009-9128-x. Epub 2009 Jul 10.

Curcumin and cancer cells: how many ways can curry kill tumor cells selectively?

Jayaraj Ravindran  1 , Sahdeo Prasad, Bharat B Aggarwal
Affiliations
Review

Curcumin and cancer cells: how many ways can curry kill tumor cells selectively?

Jayaraj Ravindran et al. AAPS J. 2009 Sep.

Abstract

Cancer is a hyperproliferative disorder that is usually treated by chemotherapeutic agents that are toxic not only to tumor cells but also to normal cells, so these agents produce major side effects. In addition, these agents are highly expensive and thus not affordable for most. Moreover, such agents cannot be used for cancer prevention. Traditional medicines are generally free of the deleterious side effects and usually inexpensive. Curcumin, a component of turmeric (Curcuma longa), is one such agent that is safe, affordable, and efficacious. How curcumin kills tumor cells is the focus of this review. We show that curcumin modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin D1, c-myc), cell survival pathway (Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1), caspase activation pathway (caspase-8, 3, 9), tumor suppressor pathway (p53, p21) death receptor pathway (DR4, DR5), mitochondrial pathways, and protein kinase pathway (JNK, Akt, and AMPK). How curcumin selectively kills tumor cells, and not normal cells, is also described in detail.

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Figures

Fig. 1
Fig. 1
Modulation of various cell death pathways by curcumin. Targets up-regulated by curcumin are in a blue box, those down-regulated are in a yellow box, and those unaffected are in a white box. AP-1 activator protein-1, AMPK 5' adenosine monophosphate-activated protein kinase, BID BH3 interacting domain death agonist, BIM BCL2-like 11 (apoptosis facilitator), cFLIP cellular FLICE-like inhibitory protein, FADD Fas-associated protein with Death Domain, DR4 death receptor 4, DR5 death receptor 5, EGFR epithelial growth factor receptor, IAP inhibitor of apoptosis protein, IL-6 interleukin-6, JNK c-Jun N-terminal kinase, mTOR mammalian target of rapamycin, NF-kB nuclear factor-kB, PI3K phosphoinositide 3-kinase, STAT3 signal transducer and activator of transcription 3, XIAP X-linked IAP
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