Induction of apoptosis by gallic acid in lung cancer cells

Ohno, Yasushi; Fukuda, Kazunori; Takemura, Genzou; Toyota, Miki; Watanabe, Minoru; Yasuda, Norio; Qiu, Xinbin; Maruyama, Rumi; Akao, Seigou; Gotou, Kouji; Fujiwara, Takako; Fujiwara, Hisayoshi

doi:10.1097/00001813-199910000-00008

Cited by 94 publications

(58 citation statements)

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“…Because the antiproliferative or antigrowth activities of gallic acid against lung cancer cell lines have been reported (27,28), we next wished to decipher the molecular basis of gallic acid's inhibition of the growth and proliferation of cancer cells. We first asked whether the antiproliferative effect of gallic acid was mediated through the downregulation of cell survival or proliferative gene products mainly regulated by NF-κB.…”

Section: Gallic Acid Suppresses the Expression Of Nf-κb-regulated Antmentioning

confidence: 99%

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

Choi

Lee

Jung

et al. 2009

Molecular Cancer Research

146

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Although multiple studies have revealed that gallic acid plays an important role in the inhibition of malignant transformation, cancer development, and inflammation, the molecular mechanism of gallic acid in inflammatory diseases is still unclear. In this study, we identified gallic acid from Rosa rugosa as a histone acetyltransferase (HAT) inhibitor with global specificity for the majority of HAT enzymes, but with no activity toward epigenetic enzymes including sirtuin (silent mating type information regulation 2 homologue) 1 (S. cerevisiae), histone deacetylase, and histone methyltransferase. Enzyme kinetic studies indicated that gallic acid uncompetitively inhibits p300/CBP-dependent HAT activities. We found that gallic acid inhibits p300-induced p65 acetylation, both in vitro and in vivo, increases the level of cytosolic IκBα, prevents lipopolysaccharide (LPS)-induced p65 translocation to the nucleus, and suppresses LPS-induced nuclear factor-κB activation in A549 lung cancer cells. We have also shown that gallic acid treatment inhibits the acetylation of p65 and the LPS-induced serum levels of interleukin-6 in vivo. Importantly, gallic acid generally inhibited inflammatory responses caused by other stimuli, including LPS, IFN-γ, and interleukin-1β, and further downregulated the expression of nuclear factor-κB-regulated antiapoptotic genes. These results show the crucial role of acetylation in the development of inflammatory diseases. (Mol Cancer Res 2009;7(12):2011-21)

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Section: Gallic Acid Suppresses the Expression Of Nf-κb-regulated Antmentioning

confidence: 99%

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

Choi

Lee

Jung

et al. 2009

Molecular Cancer Research

146

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“…its various biological activities, such as anti-bacterial (3), anti-viral (4) and anti-inflammatory (5), have been reported, and the anti-cancer activity of Ga has been reported in various types of cancer cells, such as prostate (6), lung (7,8), gastric, colon, breast, cervical and esophageal (9). cell death induced by Ga is associated with oxidative stress derived from reactive oxygen species (roS), mitochondrial dysfunction and an increase in intracellular ca 2+ level (10,11).…”

Section: Introductionmentioning

confidence: 99%

MAPK inhibitors differentially affect gallic acid-induced human pulmonary fibroblast cell growth inhibition

Park

2010

Mol Med Rep

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Abstract. Gallic acid (Ga) has various biological properties, including an anti-cancer effect. However, little is known about the toxicological effect of Ga in primary normal cells in relation to mitogen-activated protein kinase (MaPK) signaling. in this study, we investigated the effects of MaPK (MeK, JnK or p38) inhibitors on Ga-treated human pulmonary fibroblast (HPF) cells in relation to cell growth inhibition, cell death, reactive oxygen species (roS) and glutathione (GSH). GA induced HPF cell growth inhibition and cell death at 24 h, which was accompanied by the loss of mitochondrial membrane potential (MMP; ∆ψ m ). Ga increased roS levels and GSH-depleted cell numbers in the HPF cells. The MEK inhibitor did not affect cell growth inhibition, cell death, roS and GSH levels in the GA-treated HPF cells. The JNK inhibitor slightly enhanced cell growth inhibition by Ga, while the p38 inhibitor significantly prevented the growth inhibition. Both JnK and p38 inhibitors did not affect cell death, roS and GSH levels in the GA-treated HPF cells. In conclusion, MaPK inhibitors differentially affected the growth inhibition of GA-treated HPF cells, which were not related to cell death, roS and GSH levels.

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“…12 Moreover, resveratrol and other polyphenols such as quercetin were also shown to enhance endothelial nitric oxide synthase 13 and to reduce the expression of the procoagulant activity of vascular cells. 14 Our attention was therefore drawn to gallic acid (GA), a major antioxidant constituent in red wine that has been shown to display in situ or as an alkyl derivative antioxidant 15 and anticarcinogenic 16 activity. Interestingly, we previously found that derivatization of peptide antagonists for human P-selectin with GA enhanced their affinity for P-selectin Ͼ500-fold.…”

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confidence: 99%

Gallic Acid Antagonizes P-Selectin–Mediated Platelet–Leukocyte Interactions

et al. 2005

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Background-Current paradigm attributes the low incidence of cardiovascular disorders in Mediterranean countries despite a high saturated fat intake, the "French paradox," to the antioxidant capacity of red wine polyphenols.Conceivably, other antiinflammatory pathways may contribute to at least a similar extent to the atheroprotective activity of these polyphenols. We have investigated whether gallic acid (GA), an abundant red wine polyphenol, modulates the activity of P-selectin, an adhesion molecule that is critically involved in the recruitment of inflammatory cells to the vessel wall and thus in atherosclerosis. Methods and Results-GA potently inhibited the binding of a peptide antagonist (IC 50 , 7.2 mol/L) and biotin-PAA-Le a -SO 3 H, an established high-affinity ligand, to P-selectin (IC 50 , 85 mol/L). Under dynamic flow conditions, GA markedly and dose dependently attenuated the rolling of monocytic HL60 cells over P-selectin-transfected Chinese hamster ovary cells (EC 50 , 14.5 mol/L) while increasing the velocity of P-selectin-dependent rolling of human blood leukocytes over a platelet monolayer. In vivo tests established that GA administration to normolipidemic C57/Bl6 and aged atherosclerotic apolipoprotein E-deficient mice impaired the baseline rolling of conjugates between activated platelets and circulating monocytes over femoral vein endothelium, as judged by online video microscopy (ED 50 , 1.7Ϯ0.3 and 1.5Ϯ0.4 mg · kg Ϫ1 · h Ϫ1 , respectively). Conclusions-Our findings provide a solid mechanistic foundation through which GA intervenes in major inflammatory pathobiologies by binding and antagonizing P-selectin.

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Induction of apoptosis by gallic acid in lung cancer cells

Cited by 94 publications

References 0 publications

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

MAPK inhibitors differentially affect gallic acid-induced human pulmonary fibroblast cell growth inhibition

Gallic Acid Antagonizes P-Selectin–Mediated Platelet–Leukocyte Interactions

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