• Corpus ID: 8591797

Inhibitory effect of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by 12-O-tetradecanoylphorbol-13-acetate.

  title={Inhibitory effect of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by 12-O-tetradecanoylphorbol-13-acetate.},
  author={M. T. Huang and Robert C Smart and C. Q. Wong and Allan H. Conney},
  journal={Cancer research},
  volume={48 21},
The effects of topically applied curcumin, chlorogenic acid, caffeic acid, and ferulic acid on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice. Topical application of 0.5, 1, 3, or 10 mumol of curcumin inhibited by 31, 46, 84, or 98%, respectively, the induction of epidermal ornithine decarboxylase activity by 5 nmol of TPA. In an additional study, the… 

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Inhibitory effects of curcumin on in vitro lipoxygenase and cyclooxygenase activities in mouse epidermis.

The inhibitory effects of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on TPA-induced tumor promotion in mouse epidermis parallel their inhibitory effect on T PA-induced epidermal inflammation and epider mal lipoxygenase and cyclo oxygengenase activities.

Inhibitory effects of caffeic acid phenethyl ester (CAPE) on 12-O-tetradecanoylphorbol-13-acetate-induced tumor promotion in mouse skin and the synthesis of DNA, RNA and protein in HeLa cells.

The results indicate a potent inhibitory effect of CAPE on TPA-induced tumor promotion and Tpa-induced formation of HMdU in DNA of mouse skin as well as an inhibitory effects ofCAPE on the synthesis of DNA, RNA and protein in culture HeLa cells.

Curcumin inhibits phorbol ester-induced expression of cyclooxygenase-2 in mouse skin through suppression of extracellular signal-regulated kinase activity and NF-kappaB activation.

Recently, there have been considerable efforts to search for naturally occurring substances for the intervention of carcinogenesis. Many components derived from dietary or medicinal plants have been

Some Perspectives on Dietary Inhibition of Carcinogenesis: Studies with Curcumin and Tea

  • A. ConneyY. Lou M.-T. Huang
  • Biology, Medicine
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1997
Although curcumin alone had little or no effect on cellular differentiation, when it was combined with all-trans retinoic acid or 1α,25-dihydroxyvitamin D3 a synergistic effect was observed and it is possible that many dietary chemicals in fruits, vegetables, and other edible plants can prevent cancer by synergizing with endogenously produced stimulators of differentiation.

Evaluation of the potential of cancer chemopreventive activity mediated by inhibition of 12-O-tetradecanoyl phorbol 13-acetate-induced ornithine decarboxylase activity

A chemically diverse group of compounds was included in the evaluation, such as flavonoids, retinoids, isothiocyanates, sulfur-containing compounds and phenolic antioxidant compounds, and showed potent inhibitory effects in this process to understand the cancer chemopreventive potential mediated by these substances.

Inhibitory effects of curcumin on tumorigenesis in mice

Curcumin is a strong inhibitor of arachidonic acid‐induced edema of mouse ears in vivo and epidermal cyclo oxygengenase and lipoxygenase activities in vitro, and poor circulating bioavailability of curcumin may account for the lack of lung and breast carcinogenesis inhibition.

Inhibitory effects of 1,3-bis-(2-substituted-phenyl)-propane-1,3-dione, β-diketone structural analogues of curcumin, on chemical-induced tumor promotion and inflammation in mouse skin.

1,3-bis-(2-acetoxyphenyl-propane-1-3-dione) merits a valuable anti-inflammatory agent substituting aspirin in therapeutic treatment as well prevention of cancer.

A simple phenolic antioxidant protocatechuic acid enhances tumor promotion and oxidative stress in female ICR mouse skin: dose-and timing-dependent enhancement and involvement of bioactivation by tyrosinase.

Results suggested that tyrosinase-dependent oxidative metabolism of PA was at least partially involved in the enhanced effects of PA on TPA-induced inflammatory responses and thus tumor promotion.



Inhibition of 12-O-tetradecanoylphorbol-13-acetate induction of ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse skin by ascorbic acid and ascorbyl palmitate.

The topical application of relatively small doses of ascorbyl palmitate had a marked inhibitory effect on TPA-induced ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse epidermis.

Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced tumor promotion and ornithine decarboxylase activity by quercetin: possible involvement of lipoxygenase inhibition.

The results suggest that the inhibition of lipoxygenase by quercetin is one of the major actions of the above agent to inhibit tumor promotion and TPA-induced ODC activity.

Effects of flavonoids and antioxidants on 12-O-tetradecanoyl-phorbol-13-acetate-caused epidermal ornithine decarboxylase induction and tumor promotion in relation to lipoxygenase inhibition by these compounds.

The inhibitory effects of flavonoids and antioxidants on the TPA-caused ODC induction and tumor promotion were roughly parallel with their activities of lipoxygenase inhibition.

Vitamin A acid (retinoic acid), a potent inhibitor of 12-O-tetradecanoyl-phorbol-13-acetate-induced ornithine decarboxylase activity in mouse epidermis.

The ability of retinoids to inhibit tetradecanoyl-phorbol-acetate-induced epidermal ornithine decarboxylase activity correlated with their ability to inhibit skin tumor promotion.

Inhibition by 2(3)-tert-butyl-4-hydroxyanisole and other antioxidants of epidermal ornithine decarboxylase activity induced by 12-O-tetradecanoylphorbol-13-acetate.

Results demonstrate an early and direct inhibition of TPA-induced ODC activity by lipophilic phenolic antioxidants and suggest a role for reactive oxygen and/or free radical species in tumor promotion.

sn-1,2-Diacylglycerols mimic the effects of 12-O-tetradecanoylphorbol-13-acetate in vivo by inducing biochemical changes associated with tumor promotion in mouse epidermis.

Several sn-1,2-diacylglycerols mimic TPA in vivo with respect to their effects on certain biochemical parameters associated with tumor promotion in mouse skin, and these effects are determined by measuring the incorporation of [3H]thymidine into epidermal DNA.

Inhibitory effects of glutathione level-raising agents and D-alpha-tocopherol on ornithine decarboxylase induction and mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate.

The results suggest that GSH level-raising agents and other antioxidants might inhibit by diverse means the effects of TPA on GSH metabolism and skin tumor promotion.

Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced epidermal ornithine decarboxylase activity by lipoxygenase inhibitors: possible role of product(s) of lipoxygenase pathway.

The above findings strongly suggest that not only cyclooxygenase product but also lipoxygen enzyme product are involved in the mechanism of ODC induction in mouse epidermis, and a lack of either cyclo oxygenase product or lipoxyGENase product causes a failure of O DC induction by TPA.

Fluocinolone acetonide: a potent inhibitor of mouse skin tumor promotion and epidermal DNA synthesis.

Phorbol ester induction of 8-lipoxygenase in inbred SENCAR (SSIN) but not C57BL/6J mice correlated with hyperplasia, edema, and oxidant generation but not ornithine decarboxylase induction.

Several responses suggested to be critical components of phorbol ester tumor promotion were compared in 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion-sensitive SSIN and TPA promotion-resistant C57BL/6J mice, and oxidant generation or possibly 8-lipoxygenase activity may be the basis for the sensitivity or resistance to TPA as a hyperplasiogen and as a tumor promoter.