Inhibitory effect of curcumin and some related dietary compounds on tumor promotion and arachidonic acid metabolism in mouse skin

Conney, Allan H.; Lysz, Thomas W.; Ferraro, Thomas; Abidi, Tanveer F.; Manchand, Percy S.; Laskin, Jeffrey D.; Huang, Mou‐Tuan

doi:10.1016/0065-2571(91)90025-h

Cited by 161 publications

(85 citation statements)

References 12 publications

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“…24). Owing to their potent inhibitory activity on arachidonic acid release and metabolism both cycloxygenase and lipoxygenase pathways are inhibited by these natural products (43). Anticancer activity of curcuminoids has been associated with inhibition of c-myc, c-jun, and c-fos oncogene expression, and signal transduction studies have revealed that this inhibition occurs via inhibition of c-Jun N-terminal kinase activation (44).…”

Section: Curcuminoids Reduce the Angioproliferative Response In Vivomentioning

confidence: 99%

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

Mohan¹,

Sivak²,

Ashton³

et al. 2000

Journal of Biological Chemistry

231

126

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We have studied mechanisms controlling activation of the gelatinase B gene (matrix metalloproteinase-9) by fibroblast growth factor-2 (FGF-2) during angiogenesis, and the effects of the natural product curcuminoids on this process. Using a transgenic mouse (line 3445) harboring a gelatinase B promoter/lacZ fusion gene, we demonstrate FGF-2 stimulation of reporter gene expression in endothelial cells of invading neocapillaries in the corneal micropocket assay. Using cultured corneal cells, we show that FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-B and that AP-1 stimulation is inhibited by curcuminoids. We further show that induction of gelatinase B transcriptional promoter activity in response to FGF-2 is dependent on AP-1 but not NF-B response elements and that promoter activity is also inhibited by curcuminoids. In rabbit corneas, the angiogenic response induced by implantation of an FGF-2 pellet is inhibited by the coimplantation of a curcuminoid pellet, and this correlates with inhibition of endogenous gelatinase B expression induced by FGF-2. Angiostatic efficacy in the cornea is also observed when curcuminoids are provided to mice in the diet. Our findings provide evidence that curcuminoids target the FGF-2 angiogenic signaling pathway and inhibit expression of gelatinase B in the angiogenic process.

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Section: Curcuminoids Reduce the Angioproliferative Response In Vivomentioning

confidence: 99%

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

Mohan¹,

Sivak²,

Ashton³

et al. 2000

Journal of Biological Chemistry

231

126

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“…Curcumin has been shown to be chemopreventive and chemotherapeutic by blocking tumor initiation (8)(9)(10)(11)(12)(13) induced by benzo[a]pyrene and 7,12 dimethylbenz[a]anthracene; it suppressed phorphol ester-induced tumor promotion; suppressed carcinogenesis of the skin, forestomach; and colon in mice. It has been shown to prevent cancer in colon, skin stomach, duodenum following oral administration (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Effect of curcumin on irradiated and estrogen-transformed human breast cell lines

Calaf

Echiburú-Chau²,

Wen³

et al. 2011

Int J Oncol

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Abstract. Curcumin (diferuloyl methane) is a well known antioxidant that exerts antiproliferative and apoptotic effects. Curcumin effect was evaluated in a breast cancer model that was developed using the immortalized breast epithelial cell line MCF-10F after exposure to low doses of high LET (linear energy transfer) α particles (150 keV/µm) of radiation, and subsequently cultured in the presence of 17β-estradiol (estrogen). This model consisted of human breast epithelial cells in different stages of transformation: i) MCF-10F; ii) Estrogen cell line; iii) a malignant Alpha3 cell line; iv) a malignant and tumorigenic, Alpha5 cell line; and v) a cell line derived from Alpha5 injected into the nude mice that gave rise to Tumor2 cell line. Curcumin decreased anchorage-independent growh in transformed breast cancer cell lines in comparison to their counterparts and increased the percentage of cells from G 0 /G 1 with a concomitant increase in G 2 /M phases, as well as a decrease in PCNA and Rho-A protein expression. Among the oncogenes, c-Ha-Ras and Ras homologous A (Rho-A) are important cell signaling factors for malignant transformation and to reach their active GTP bound state, Ras proteins must first release bound GDP mediated by a guanine nucleotide releasing factor (GRF). Then curcumin decrease RasGRF1 protein expression in malignant cell lines. Further, differential expression levels of cleaved (ADP) ribose polymerase 1 (PARP-1) and phosphorylated histone H2AX (γ-H2AX) were observed after curcumin treatment. It seems that PARP-1 similar to H2AX, confers cellular protection against radiation and estrogen-induced DNA damage mediated by curcumin. Therefore, targeting either PARP-1 or H2AX may provide an effective way of maximizing the therapeutic value of antioxidants for cancer prevention.

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“…Curcumin is known for its wide ranges of beneficial effects, such as antiinflammatory and cancer chemopreventing activities. 25 These activities include antioxidation, 26 suppression of c-jun/AP-1, 27 inhibition of prostaglandin biosynthesis 28 and inhibition of the activity and expression of the enzyme cyclooxygenase. 29,30 A second NF-kB inhibitor is caffeic acid phenethyl ester (CAPE).…”

Section: Introductionmentioning

confidence: 99%

Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury

Land¹,

Blijlevens

Marteijn³

et al. 2003

Leukemia

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The inhibition of nuclear factor kappa B (NF-jB) by, for instance, curcumin is becoming an important new approach in combination with chemotherapy or irradiation for the treatment of a variety of cancers including haematological malignancies. A dose-limiting side effect of anticancer therapy in the gastrointestinal tract is mucosal barrier injury. It is hypothesised that mucosal barrier injury is initiated and amplified by proinflammatory-and NF-jB-regulated mediators. Therefore, the effect of NF-jB inhibition was studied in the onset of mucosal barrier injury. In response to cytostatic drug treatment (arabinoside cytosine (Ara-C) and methotrexate (MTX)), NF-jB was activated in intestinal epithelial cells (IEC-6) resulting in an NF-jB-related induction of tumour necrosis factor alpha and monocyte chemoattractant protein-1. NF-jB inhibition increased the susceptibility of IEC-6 cells to Ara-C as well as MTX-induced cell death when obtained by the addition of caffeic acid phenethyl ester (CAPE), but not using curcumin. In an animal model for MTX-induced mucosal barrier injury, the induction of NF-jB-related cytokines and chemokines was detected upon treatment with MTX. Despite increased susceptibility shown in vitro, the inhibition of NF-jB resulted in a partial amelioration of villous atrophy normally seen in the small intestine upon MTX treatment. These results show that the inhibition of NF-jB does not increase intestinal side effects of the anticancer treatment, suggesting a safe use of curcumin and CAPE in combination with anticancer treatment.

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Inhibitory effect of curcumin and some related dietary compounds on tumor promotion and arachidonic acid metabolism in mouse skin

Cited by 161 publications

References 12 publications

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

Curcuminoids Inhibit the Angiogenic Response Stimulated by Fibroblast Growth Factor-2, Including Expression of Matrix Metalloproteinase Gelatinase B

Effect of curcumin on irradiated and estrogen-transformed human breast cell lines

Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury

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