Chemoprevention of Colon Cancer by Dietary Curcumin

Rao, Chinthalapally V.; Rivenson, Abraham; Simi, Barbara; Reddy, Bandaru S.

doi:10.1111/j.1749-6632.1995.tb12122.x

Cited by 105 publications

(94 citation statements)

References 5 publications

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“…prostaglandins, inhibit apoptosis, diminish immune surveillance, and increase the invasiveness of malignant cells (14 -16). These conclusions are consistent with evidence that inhibitors of COX-2 are chemopreventive against cancers of the colon and upper gastrointestinal tract in experimental animals (45)(46)(47)(48) and in humans (49,50).…”

Section: Discussionsupporting

confidence: 79%

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Zhang¹,

Subbaramaiah²,

Altorki³

et al. 1998

Journal of Biological Chemistry

188

125

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Section: Discussionsupporting

confidence: 79%

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Zhang¹,

Subbaramaiah²,

Altorki³

et al. 1998

Journal of Biological Chemistry

188

125

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“…Curcumin is a dietary compound with the known properties of antioxidation, anti-in¯ammation, and anticarcinogenesis (Huang et al, 1994;1988;Rao et al, 1995;Ruby et al, 1995;Singh and Aggarwal, 1995). Curcumin blocks c-jun expression and NF-kB activation induced by various agents (Hanazawa et al, 1993;Huang et al, 1991;Singh and Aggarwal, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…The anticarcinogenic e ects of this compound are demonstrated by its ability to inhibit tumor initiation by azoxymethane, benzpyrene and 7,12-dimethyl-benz(a)anthracene, and to suppress tumor promotion by phorbol esters (Huang et al, 1994(Huang et al, , 1988Rao et al, 1995). It has been shown that curcumin strongly inhibits both c-Jun and NF-kB activation by PMA or tumor necrosis factor-a (TNF-a) treatments (Hanazawa et al, 1993;Huang et al, 1991;Singh and Aggarwal, 1995).…”

mentioning

confidence: 99%

Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin

1998

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Curcumin, a dietary pigment in curry, suppresses tumor initiation and tumor promotion. Curcumin is also a potent inhibitor for AP-1 and NF-kB activation. In this report, we show that curcumin inhibits JNK activation by various agonists including PMA plus ionomycin, anisomycin, UV-C, g radiation, TNF-a, and sodium orthovanadate. Although both JNK and ERK activation by phorbol 12-myristate 13-acetate (PMA) plus ionomycin were suppressed by curcumin, the JNK pathway was more sensitive. The IC 50 (50% inhibition concentration) of curcumin was between 5 ± 10 mM for JNK activation and was 20 mM for ERK activation. In transfection assays, curcumin moderately suppressed MEKK1-induced JNK activation; however, it e ectively blocked JNK activation caused by co-transfection of TAK1, GCK, or HPK1. Curcumin did not directly inhibit JNK, SEK1, MEKK1 or HPK1 activity. Although curcumin suppressed TAK1 and GCK activities at high concentrations, this inhibition cannot fully account for the JNK inhibition by curcumin in vivo. Our data suggest that curcumin may a ect the JNK pathway by interfering with the signaling molecule(s) at the same level or proximally upstream of the MAPKKK level. Taken together, the inhibition of the MEKK1-JNK pathway reveals a possible mechanism of suppression of AP-1 and NF-kB signaling by curcumin, and may explain the potent anti-in¯ammatory and anti-carcinogenic e ects of this chemical.

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“…There is a reduction in the relative risk of colorectal cancer in individuals taking non-steroidal anti-inflammatory drugs (2,3). COX-2 levels are increased in ϳ90% of human colorectal cancers and ϳ50% of premalignant adenomas (1).…”

Section: Discussionmentioning

confidence: 99%

Potential Role of Microsomal Prostaglandin E Synthase-1 in Tumorigenesis

Kamei

Murakami

Nakatani

et al. 2003

Journal of Biological Chemistry

181

168

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Microsomal prostaglandin E 2 synthase-1 (mPGES-1) is a stimulus-inducible enzyme that functions downstream of cyclooxygenase (COX)-2 in the PGE 2 -biosynthetic pathway. Given the accumulating evidence that COX-2-derived PGE 2 participates in the development of various tumors, including colorectal cancer, we herein examined the potential involvement of mPGES-1 in tumorigenesis. Immunohistochemical analyses demonstrated the expression of both COX-2 and mPGES-1 in human colon cancer tissues. HCA-7, a human colorectal adenocarcinoma cell line that displays COX-2-and PGE 2 -dependent proliferation, expressed both COX-2 and mPGES-1 constitutively. Treatment of HCA-7 cells with an mPGES-1 inhibitor or antisense oligonucleotide attenuated, whereas overexpression of mPGES-1 accelerated, PGE 2 production and cell proliferation. Moreover, cotransfection of COX-2 and mPGES-1 into HEK293 cells resulted in cellular transformation manifested by colony formation in soft agar culture and tumor formation when implanted subcutaneously into nude mice. cDNA array analyses revealed that this mPGES-1-directed cellular transformation was accompanied by changes in the expression of a variety of genes related to proliferation, morphology, adhesion, and the cell cycle. These results collectively suggest that aberrant expression of mPGES-1 in combination with COX-2 can contribute to tumorigenesis.Clinical, genetic, and biochemical evidence has suggested that prostaglandin (PG) 1 E 2 produced via the cyclooxygenase (COX)-2-dependent pathway plays a crucial role in the development of colorectal cancer and possibly other cancers (1). Non-steroidal anti-inflammatory drugs, which inhibit COX-2, reduce the incidence of colorectal cancer (2-4). The major prostanoid produced by several types of cancer is PGE 2 , which is produced by three biosynthetic reactions involving phospholipase A 2 (PLA 2 ), COX, and terminal PGE 2 synthase (PGES). PGE 2 promotes survival and motility of colon cancer cells in vitro and promotes tumorigenesis and angiogenesis in vivo (5-7). High levels of constitutive expression of COX-2 have been found in various cancer cells and tissues (8,9), and studies employing overexpression, antisense suppression, and specific inhibitors of COX-2 have demonstrated that COX-2 contributes to the progression of several types of cancer (10 -12).More direct evidence for the role of COX-2 and its product PGE 2 in colorectal tumorigenesis has been provided by gene targeting studies. Gene disruption of either COX-2 (13) or the PGE receptor EP2 (14) results in reduction of the number and size of intestinal polyps in Apc mutant mice, a model for human familial adenomatous polyposis. In another model, disruption of the genes for the PGE receptors EP1 (15) or EP4 (16) suppresses the development of colorectal cancer induced by carcinogen. Moreover, gene knockout of cytosolic PLA 2 ␣ (cPLA 2 ␣), which supplies the substrate arachidonic acid to COX-2, also leads to reduced polyposis in Apc mutant mice (17,18).PGES catalyzes the conversion of PGH 2 ...

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Chemoprevention of Colon Cancer by Dietary Curcumin

Cited by 105 publications

References 5 publications

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Dihydroxy Bile Acids Activate the Transcription of Cyclooxygenase-2

Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin

Potential Role of Microsomal Prostaglandin E Synthase-1 in Tumorigenesis

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