Disease relevance of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• Previous work from this laboratory established that caffeic acid esters, present in the propolis of honey bee hives, are potent inhibitors of human colon tumor cell growth, suggesting that these compounds may possess antitumor activity against colon carcinogenesis [1].
• Previous studies from this laboratory have established that caffeic acid esters present in propolis, a natural resin produced by honey bees, are potent inhibitors of human colon adenocarcinoma cell growth, carcinogen-induced biochemical changes, and preneoplastic lesions in the rat colon [2].
• Caffeic acid phenethyl ester induces apoptosis by inhibition of NFkappaB and activation of Fas in human breast cancer MCF-7 cells [3].
• Recombinant COMT expressed in Escherichia coli exhibited the highest V(max)/K(m) values with 5-hydroxyconiferaldehyde and caffeoyl aldehyde, and the lowest with caffeic acid [4].
• The protective effects of selected members from a series of caffeic acid esters and flavonoids were tested in various toxicity paradigms using U937 cells, previously shown to be sensitive to either iron chelators or bona fide radical scavengers or to both classes of compounds [5].

High impact information on 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• COMT is unlikely to catalyze the in vivo methylation of caffeic acid during lignin biosynthesis [6].
• Downregulation of caffeic acid 3-O-methyltransferase and caffeoyl CoA 3-O-methyltransferase in transgenic alfalfa. impacts on lignin structure and implications for the biosynthesis of G and S lignin [6].
• Caffeic acid phenethyl ester is a potent and specific inhibitor of activation of nuclear transcription factor NF-kappa B [7].
• Inhibitory effects of caffeic acid phenethyl ester on the activity and expression of cyclooxygenase-2 in human oral epithelial cells and in a rat model of inflammation [8].
• Neuroprotection was observed with the 5-LO inhibitor, caffeic acid [9].

Chemical compound and disease context of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• Using cultured MCF-7 and MAD-MB-231 human breast cancer cells, we also demonstrated that treatment of these cells with caffeic acid or chlorogenic acid partially inhibited the methylation of the promoter region of the RARbeta gene [10].
• Involvement of tumor suppressor protein p53 and p38 MAPK in caffeic acid phenethyl ester-induced apoptosis of C6 glioma cells [11].
• Three of four natural compounds, which are caffeic acid, eupatilin and 4'-demethyleupatilin, isolated from Chinese plant, Artemisia rubripes Nakai selectively inhibited 5-lipoxygenase of cultured mastocytoma cells [12].
• We report that the cDNA clone (Accession No. U70424), previously isolated from Arabidopsis thaliana as encoding a caffeic acid/5-hydroxyferulic acid O-methyltransferase (OMT) (1), has now been overexpressed in Escherichia coli BL21 and its recombinant protein identified as a novel flavonol 3'-OMT [13].
• The mutagenicity of 4 coffee flavor ingredients (chlorogenic acid, caffeic acid, pyrazine, and trigonelline) was evaluated in the Salmonella plate incorporation assay and mouse lymphoma L5178Y TK +/- assay [14].

Biological context of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• Investigation of the mechanism responsible for this enhancement of HCV replicon expression demonstrated that morphine activated NF-kappaB promoter and that caffeic acid phenethyl ester, a specific inhibitor of the activation of NF-kappaB, blocked morphine-activated HCV RNA expression [15].
• Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats [16].
• This effect seems to be due to the ability of caffeic acid to reduce glutathione depletion and to inhibit lipid peroxidation during tBOOH treatment [17].
• Thus, ferulic, isoferulic, and dihydroferulic acids are specific biomarkers for the bioavailability and metabolism of dietary caffeic acid esters [18].
• Developmental expression and substrate specificities of alfalfa caffeic acid 3-O-methyltransferase and caffeoyl coenzyme A 3-O-methyltransferase in relation to lignification [19].

Anatomical context of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• Thus, the current investigation showed caffeic acid to exert carcinogenic activity for the forestomach squamous cell epithelium in both sexes of F344 rats and C57BL/6N x C3H/HeN F1 mice, for the renal tubular cell in male rats and female mice, and for the alveolar type II cell in male mice [20].
• In addition, the p43-stimulated IL-12 induction and NF-kappaB DNA-binding activity were significantly suppressed by caffeic acid phenethyl ester and BAY11-7082, both inhibitors of NF-kappaB activation, indicating that p43 induced the production of IL-12 in macrophages mainly via the activation of NF-kappaB [21].
• Modulation of ceramide-induced NF-kappaB binding activity and apoptotic response by caffeic acid in U937 cells: comparison with other antioxidants [22].
• In this work, homozygous tobacco (Nicotiana tabacum) lines transformed with cinnamoyl-coenzyme A reductase (CCR) or caffeic acid/5-hydroxy ferulic acid-O-methyltransferase I (COMT I) antisense sequences have been crossed and enzyme activities, lignin synthesis, and cell wall structure of the progeny have been analyzed [23].
• In whole-cell and single-channel patch-clamp recordings from bovine adrenal fasciculata cells, it was discovered that selected caffeic acid derivatives dramatically enhanced the activity of background TREK-1 K+ channels [24].

Associations of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)- with other chemical compounds

• In vitro rat brain protein kinase C activity was not affected by 50-200 microM curcumin, chlorogenic acid, caffeic acid, or ferulic acid [25].
• Our in vivo results support the recently obtained in vitro enzymatic data that suggest that the route from caffeic acid to sinapic acid is not used for lignin biosynthesis [26].
• We have found that Arabidopsis CYP98A3, also a P450, could hydroxylate p-coumaric acid to caffeic acid in vivo when expressed in yeast (Saccharomyces cerevisiae) cells, albeit very slowly [27].
• Because inflammatory stimuli induce iNOS to generate large amounts of nitric oxide (NO), intracellular NO levels in the presence of Bay 11-7082, NAC, and caffeic acid methyl ester were estimated [28].
• These results indicate that COMT is unlikely to methylate caffeic acid during lignin biosynthesis in vivo, and provide enzymatic evidence for an alternative pathway to monolignols involving methylation of caffeoyl aldehyde and/or caffeoyl alcohol by COMT [4].

Gene context of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• The NF-kappaB inhibitor caffeic acid phenethyl ester inhibited production of both tumor necrosis factor alpha and interleukin-10 (IL-10) induced by Leishmania amastigotes in differentiated U937 cells [29].
• Caffeic acid attenuates the decrease in cortical BDNF mRNA expression induced by exposure to forced swimming stress in mice [30].
• The present study examined whether caffeic acid affects the expression levels of BDNF and TrkB mRNA in brain regions of mice subjected to a forced swimming test [30].
• In this study, we explored the effects of caffeic acid phenethyl ester on growth, cell cycle, apoptosis and beta-catenin/T-cell factor signaling in human colon cancer cells [31].
• In this study, we investigated whether caffeic acid regulates Rac1 GTPase activity, a partner of NADPH oxidase [32].

Analytical, diagnostic and therapeutic context of 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-

• An important role for nuclear factor kappaB (NF-kappaB) was also demonstrated using the inhibitor caffeic acid phenethyl ester and electrophoretic mobility shift assays [33].
• Pulsed field gel electrophoresis showed that caffeic acid induced DNA strand breaks in cultured human cells in the presence of Mn(II) [34].
• The products of enzymic oxidation of caffeic acid were analyzed and isolated by HPLC with diode array detection [35].
• Product analysis of caffeic acid oxidation by on-line electrochemistry/electrospray ionization mass spectrometry [36].
• Caffeic acid induced a significant reduction of the blood glucose and glycosylated hemoglobin levels than the control group [37].

References