Derivatives of Gallic Acid Induce Apoptosis in Tumoral Cell Lines and Inhibit Lymphocyte Proliferation

Serrano, Antonio; Palacios, Carmen; Roy, Garbiñe; Cespón, Constantino; Villar, Luisa M.; Nocito, Mercedes; González-Porqué, Pedro

doi:10.1006/abbi.1997.0474

Cited by 176 publications

(112 citation statements)

References 17 publications

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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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“…First, LG inhibits PTKs in whole cells, crude extracts and purified form (PTK c-Src) without inhibiting serine/threonine kinases (Palacios et al, 2002) and are not affected by high ATP concentrations. This compound and other gallic acid derivatives are able to induce apoptosis in tumoral cell lines showing selectivity for rapidly growing cells (resting lymphocytes can stand much higher concentrations than mitogen-stimulated lymphocytes (Serrano et al, 1998).…”

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 95%

“…Similarly to other PTK inhibitors such as genistein (Uckun et al, 1995), herbymicin (Otani et al, 1993), staurosporin (Bossy-Wetzel et al, 1998), tyrphostins (Burger et al, 1995), etc., they show an antiproliferative effect on tumoral cell lines (Serrano et al, 1998). The most hydrophobic of the alkyl gallates (octyl and lauryl) exhibit a proapoptotic potency between 50 and 250 times higher than gallic acid for the lines tested (Serrano et al, 1998). The study of lauryl gallate (LG) on the pre-B cell lymphoma Wehi 231 line shows that it inhibits PTKs both in crude extracts and whole cells, disrupts the mitochondrial membrane potential, promotes the efflux of cytochrome c to the cytosol, activates the cascade of caspases and induces oligonucleosomal breakdown of DNA (Roy et al, 2000).…”

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confidence: 99%

“…The study of lauryl gallate (LG) on the pre-B cell lymphoma Wehi 231 line shows that it inhibits PTKs both in crude extracts and whole cells, disrupts the mitochondrial membrane potential, promotes the efflux of cytochrome c to the cytosol, activates the cascade of caspases and induces oligonucleosomal breakdown of DNA (Roy et al, 2000). Also these types of compounds seem to show a selectivity for rapidly growing cells, opening the possibility of their study as potential antitumoral agents (Serrano et al, 1998). Here, we report that LG not only prevents the formation of chemically induced skin tumours in mice but is also able to kill, selectively, tumoral cells in established tumours.…”

mentioning

confidence: 99%

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Tumoricidal activity of lauryl gallate towards chemically induced skin tumours in mice

Ortega

Sádaba

Ortiz³

et al. 2003

Br J Cancer

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Dietary hydroxybenzoic acid derivatives - nature, occurrence and dietary burden

Tomás‐Barberán

Clifford

2000

J. Sci. Food Agric.

239

110

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Quantitative data for hydroxybenzoic acids (naturally occurring and permitted additives) and their conjugates in foods and beverages are summarised. Tea, rosaceous fruits, red wines and potatoes are important sources for which more comprehensive compositional data are required. Their absorption, metabolism, toxicological evaluation and possible biological significance are discussed. There are insufficient data to properly define the dietary burdens, but it would seem that ellagic acid and gallic acid from natural sources may dominate in many cases, although the intake of added benzoic acid may be of a similar magnitude. It is pointed out that an additional, previously overlooked and possibly significant burden, particularly of benzoic acid itself, might arise as a result of the gut flora metabolism of larger‐mass dietary phenols. © 2000 Society of Chemical Industry

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Derivatives of Gallic Acid Induce Apoptosis in Tumoral Cell Lines and Inhibit Lymphocyte Proliferation

Cited by 176 publications

References 17 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

Tumoricidal activity of lauryl gallate towards chemically induced skin tumours in mice

Dietary hydroxybenzoic acid derivatives - nature, occurrence and dietary burden

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