Mechanisms of anticarcinogenic properties of curcumin: the effect of curcumin on glutathione linked detoxification enzymes in rat liver

Piper, John T.

doi:10.1016/s1357-2725(98)00015-6

Cited by 208 publications

(113 citation statements)

References 30 publications

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“…Because it is known that curcumin can induce several phase II detoxification enzyme genes and Nrf2 is critical in phase II gene induction and cancer chemoprevention, the identification of many phase II detoxification and antioxidant genes as curcumin-induced Nrf2-dependent genes in this study not only is consistent with previous studies (17,19) but also validated the results from a biological perspective. For example, the induction of selective isoform of GST and oxidative-stress response gene HO-1 is consistent with previous findings in which curcumin could induce the expression of GST (25,26) and HO-1 (19) through Nrf2/ARE pathway. The induction of cytochrome c oxidase subunits (Cox7a2 and Cox8b) and thioredoxin reductase 1 further supports the role of Nrf2 in curcumin-elicited gene expression because their promoter regions all contain putative Nrf2-binding sites.…”

Section: Discussionsupporting

confidence: 92%

“…This is supported by a previous study in which curcumin cause G 1 arrest in PC-3 cells by induction of p21 (36). Curcumin has been shown to inhibit cancer cell invasion and metastasis (25,37) by modulating integrin receptors, collagenase activity, and expression of E-cadherin. In the current study, several cadherin genes were also induced by curcumin, such as Cdh4, Cdh11, and Cdh22, in liver, although Cdh22 gene was also induced in small intestine.…”

Section: Curcumin and Global Gene Expression Profiles In Micesupporting

confidence: 75%

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Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Shen¹,

Hu³

et al. 2006

Molecular Cancer Therapeutics

158

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Curcumin has been shown to prevent and inhibit carcinogeninduced tumorigenesis in different organs of rodent carcinogenesis models. Our objective is to study global gene expression profiles elicited by curcumin in mouse liver and small intestine as well as to identify curcuminregulated nuclear factor E2-related factor 2 (Nrf2) -dependent genes. Wild-type C57BL/6J and Nrf2 knockout C57BL/6J/Nrf2(À/À) mice were given a single oral dose of curcumin at 1,000 mg/kg. Liver and small intestine were collected at 3 and 12 hours after treatments.

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Section: Discussionsupporting

confidence: 92%

Section: Curcumin and Global Gene Expression Profiles In Micesupporting

confidence: 75%

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Shen¹,

Hu³

et al. 2006

Molecular Cancer Therapeutics

158

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“…The significant enhancement in the activity of antioxidant enzymes such as glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, catalase and phase II enzymes like glutathione S-transferase and quinone reductase in the various organs of mice fed with curcumin suggests that it may contribute to the cancer chemopreventive effects observed with curcumin (Sharma 1976;Satoskar et al 1986;Huang et al 1992). These results are in agreement with the earlier reported studies of Piper et al (1998), who showed that curcumin feeding to rats resulted in the induction of glutathione linked enzymes which are known to be involved in detoxification of electrophilic product of lipid peroxidation and may contribute to the antiinflammatory and anticancer activities of curcumin.…”

Section: Discussionsupporting

confidence: 88%

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

265

145

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Dietary antioxidants protect laboratory animals against the induction of tumours by a variety of chemical carcinogens. Among possible mechanism of protection against chemical carcinogenesis could be mediated via-antioxidantdependent induction of detoxifying enzymes. Curcumin, a yellow pigment from Curcuma longa, is a major component of turmeric and is commonly used as a spice and food colouring material and exhibits antiinflammatory, antitumour, and antioxidant properties. In this study we therefore investigated the effect of dietary supplementation of curcumin on the activities of antioxidant and phase II-metabolizing enzymes involved in detoxification, and production of reactive oxygen species were quantified in ddY male mice. Dietary supplementation of curcumin (2%, w/v) to male ddY mice for 30 days significantly increased the activities of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and catalase to 189%, 179%, 189%, and 181% in liver and 143%, 134%, 167% and 115% in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.001). Parallel to these changes, curcumin feeding to mice also resulted in a considerable enhancement in the activity of phase II-metabolizing enzymes viz. glutathione S-transferase and quinone reductase to 1.7 and 1.8 times in liver and 1.1 and 1.3 times in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.01). In general, the increase in activities of antioxidant and phase II-metabolizing enzymes was more pronounced in liver as compared to kidney. The induction of such detoxifying enzymes by curcumin suggest the potential value of this compound as protective agent against chemical carcinogenesis and other forms of electrophilic toxicity. The significance of these results can be implicated in relation to cancer chemopreventive effects of curcumin against the induction of tumours in various target organs.

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“…Curcumin [1,7-bis (4-hydroxy-3-methoxyphenyl)-1,6-hepatadiene-3,5-dione; diferulolylmethane], a major constituent of the yellow spice turmeric derived from the rhizomes of Curcuma spp., is one such compound. Curcumin has been reported to have several pharmacological effects including antitumor, anti-inflammatory and antioxidant properties (2)(3)(4)(5). It is inhibitory to a broad range of tumors including colon, breast, skin, stomach, duodenum, and soft palate in rodents after oral administration.…”

Section: Introductionmentioning

confidence: 99%

Involvement of Bcl-2 family members, phosphatidylinositol 3'-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer

Shankar

Srivastava²

2007

Int J Oncol

128

140

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Abstract. Curcumin (diferulolylmethane), an active ingredient derived from the rhizome of the plant Curcuma longa, has anticancer activity in vitro and in vivo. Although curcumin possesses chemopreventive properties against several types of cancer, the molecular mechanisms by which it inhibits cell growth and induces apoptosis are not clearly understood. Our data revealed that curcumin inhibited growth and induced apoptosis in androgen-dependent and -independent prostate cancer cells, but had no effect on normal human prostate epithelial cells. Curcumin downregulated the expression of Bcl-2, and Bcl-X L and upregulated the expression of p53, Bax, Bak, PUMA, Noxa, and Bim. Curcumin upregulated the expression of p53 as well as its phosphorylation at serine 15, and acetylation in a concentration-dependent manner. Acetylation of histone H3 and H4 was increased in cells treated with curcumin, suggesting histone modification may regulate gene expression. Treatment of LNCaP cells with curcumin resulted in translocation of Bax and p53 to mitochondria, production of reactive oxygen species, drop in mitochondrial membrane potential, release of mitochondrial proteins (cytochrome c, Smac/DIABLO and Omi/HtrA2), activation of caspase-3 and induction of apoptosis. Furthermore, curcumin inhibited expression of phosphatidylinositol-3 kinase (PI3K) p110 and p85 subunits, and phosphorylation of Ser 473 AKT/PKB. Downregulation of AKT by inhibitors of PI3K (Wortmannin and LY294002) and AKT, or by dominant negative AKT increased curcumininduced apoptosis, whereas transfection of constitutively active AKT attenuated this effect. Similarly, wild-type phosphatase and tensin homolog deleted from chromosome 10 (PTEN) enhanced curcumin-induced apoptosis and, in contrast, inactive PTEN (G129E and G129R) inhibited curcumin-induced apoptosis. Overexpression of constitutively active AKT inhibited curcumin-induced p53 translocation to mitochondria, and Smac release to cytoplasm, whereas inhibition of AKT by dominant negative AKT enhanced curcumin-induced p53 translocation to mitochondria and Smac release. Our study establishes a role for AKT in modulating the direct action of p53 on the caspasedependent mitochondrial death pathway and suggests that these important biological molecules interact at the level of the mitochondria to influence curcumin sensitivity. These properties of curcumin strongly suggest that it could be used as a cancer chemopreventive agent.

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Mechanisms of anticarcinogenic properties of curcumin: the effect of curcumin on glutathione linked detoxification enzymes in rat liver

Cited by 208 publications

References 30 publications

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Involvement of Bcl-2 family members, phosphatidylinositol 3'-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer

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