Curcumin dramatically enhances retinoic acid-induced superoxide generating activity via accumulation of p47-phox and p67-phox proteins in U937 cells

Kikuchi, Hidehiko; Kuribayashi, Futoshi; Kiwaki, Naomi; Nakayama, Tatsuo

doi:10.1016/j.bbrc.2010.03.136

Cited by 22 publications

(31 citation statements)

References 24 publications

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“…In spite of their normal protective, antioxidant action, acute exposure to some polyphenols may stimulate mitochondrial (Salvi et al, 2002) and extramitochondrial (Galati et al, 2002) ROS production. In this regard, Kikuchi et al (2010) recently indicated that curcumin potentiated NADPH-derived anion superoxide generation by all-trans-retinoic acid in U937 cells, although treatment with curcumin alone was ineffective. However, our present results indicate that curcumin alone suffices to slightly stimulate anion superoxide generation in this cell line, although the exact mechanism was not investigated.…”

Section: Curcumin Increases Arsenic Trioxide and Lonidamine Toxicity 121mentioning

confidence: 99%

“…As with other plant-derived polyphenols, the proapoptotic action of curcumin has been largely attributed to the inhibition of defensive signaling pathways such as PI3K/ Akt and NF-B (Lin, 2007;Reuter et al, 2008), but other mechanisms may be equally important. For example, in spite of its normal antioxidant capacity, curcumin may per se stimulate ROS production (Woo et al, 2003;Chan et al, 2006) or potentiate ROS generation by other agents (Javvadi et al, 2008;Kikuchi et al, 2010) in different tumor cell models. Moreover, curcumin may oxidize thiol residues at the mitochondrial transition pore (mPTP), causing mitochondria dysfunction and cell death (Ligeret et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Curcumin Stimulates Reactive Oxygen Species Production and Potentiates Apoptosis Induction by the Antitumor Drugs Arsenic Trioxide and Lonidamine in Human Myeloid Leukemia Cell Lines

Sánchez¹,

Simón²,

Calviño³

et al. 2010

J Pharmacol Exp Ther

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Arsenic trioxide (ATO, Trisenox) is an important antileukemic drug, but its efficacy is frequently low when used as a single agent. Here, we demonstrate that the apoptotic action of ATO is greatly increased when combined with subcytotoxic curcumin concentrations in U937 and HL60 human acute myeloid leukemia cells, and with lower efficacy in K562 chronic myelogenous leukemia cells. Curcumin exerts similar cooperative effect with the mitochondria-targeting drug lonidamine, whereas the response is negligible in combination with the DNA-targeting drug cisplatin. Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis downregulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response. Curcumin increases anion superoxide production, and its proapoptotic action in combination with ATO and lonidamine is mimicked by pro-oxidant agents (2-methoxyestradiol and H 2 O 2 ) and prevented by antioxidant agents [Mn(III)tetrakis(4-benzoic acid)porphyrin chloride and N-acetyl-L-cysteine]. Within the assayed time period (16 -24 h), curcumin does not significantly modify p38-mitogenactivated protein kinase and c-Jun NH 2 -terminal kinase phosphorylation/activation or nuclear factor-B activity, but it greatly stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and decreases Akt phosphorylation. Experiments using mitogen-activated protein kinase kinase/ ERK inhibitors [2Ј-amino-3Ј-methoxyflavone (PD98059) and 1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene (U0126)] and phosphatidylinositol 3-kinase inhibitor 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) indicate that ERK activation does not mediate and even restrains apoptosis potentiation, whereas Akt down-regulation facilitates apoptosis generation. In summary, cotreatment with curcumin may represent a useful manner of increasing the efficacy of ATO and lonidamine as antitumor drugs in myeloid leukemia cells.

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Section: Curcumin Increases Arsenic Trioxide and Lonidamine Toxicity 121mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Curcumin Stimulates Reactive Oxygen Species Production and Potentiates Apoptosis Induction by the Antitumor Drugs Arsenic Trioxide and Lonidamine in Human Myeloid Leukemia Cell Lines

Sánchez¹,

Simón²,

Calviño³

et al. 2010

J Pharmacol Exp Ther

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“…2 was quantified by measuring SOD-sensitive chemiluminescence (CL) using Diogenes-luminol CL probes (45). Cells in PBS containing 1 mM MgCl 2 , 0.5 mM CaCl 2 , 5 mM glucose, and 0.03% BSA were stimulated with 200 ng/ml PMA at 37˚C, and the O 2 2 generation was measured by an automatic luminescence analyzer LB9505C (Berthold) or TD-20/20 luminometer (Promega).…”

Section: Omentioning

confidence: 99%

“…Fifty microliters loading buffer (0.5 M Tris-HCl [pH 6.8] containing 5% SDS and 20% glycerol) was added to the solubilized membrane fractions. Immunoblotting was performed as described (41)(42)(43)45). Data analyses were carried out using a luminescent image analyzer, LAS1000plus (Fujifilm).…”

Section: Immunoblottingmentioning

confidence: 99%

GCN5 Regulates the Superoxide-Generating System in Leukocytes Via Controlling gp91-phox Gene Expression

Kikuchi

Kuribayashi

Kiwaki

et al. 2011

The Journal of Immunology

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The superoxide anion (O2−)-generating system is an important mechanism of innate immune response against microbial infection in phagocytes and is involved in signal transduction mediated by various physiological and pathological signals in phagocytes and other cells, including B lymphocytes. The O2−-generating system is composed of five specific proteins: p22-phox, gp91-phox, p40-phox, p47-phox, p67-phox, and a small G protein, Rac. Little is known regarding epigenetic regulation of the genes constituting the O2−-generating system. In this study, by analyzing the GCN5 (one of most important histone acetyltransferases)-deficient DT40 cell line, we show that GCN5 deficiency causes loss of the O2−-generating activity. Interestingly, transcription of the gp91-phox gene was drastically downregulated (to ∼4%) in GCN5-deficient cells. To further study the involvement of GCN5 in transcriptional regulation of gp91-phox, we used in vitro differentiation system of U937 cells. When human monoblastic U937 cells were cultured in the presence of IFN-γ, transcription of gp91-phox was remarkably upregulated, and the cells were differentiated to macrophage-like cells that can produce O2−. Chromatin immunoprecipitation assay using the U937 cells during cultivation with IFN-γ revealed not only that association of GCN5 with the gp91-phox gene promoter was significantly accelerated, but also that GCN5 preferentially elevated acetylation levels of H2BK16 and H3K9 surrounding the promoter. These results suggested that GCN5 regulates the O2−-generating system in leukocytes via controlling the gp91-phox gene expression as a supervisor. Our findings obtained in this study should be useful in understanding the molecular mechanisms involved in epigenetic regulation of the O2−-generating system in leukocytes.

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“…Under influence of retinoic acid and curcumin the O 2 --producing activity of U937 leukemic human cells increased fourfold. The immunochemical analyses showed that the levels of the cyt b 558 p47 phox and p67 phox, increased seven and fourfold correspondingly in comparison with control [7], and phagocytic cytosolic isoforms of cyt b 558 p22 phox and p47phox in NADPH oxidase are comprised of 390 aminoacids with three functional domains, prolin rich domain, in particular) [8,9]. The heterodimeric membrane protein cyt b 558 , was obtained from the human phagocytes by the method of immune-affinity chromatography [10].…”

Section: Introductionmentioning

confidence: 99%

Proline Rich Polypeptide (PRP-1) Increases the Superoxide-Producing and Ferrihemoglobin Reducing Activities of Cytochrome B558 Isoforms from Human Lymphosarcoma Tissue Cells

Simonyan¹,

Galoian

Simonyan³

et al. 2011

Neurochem Res

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The two cytochromes (cyt) b(558) of acidic nature, one-95-100 kDa and another one, 60-70 kDa were isolated for the first time from the human's lymphosarcoma tissue cells using gel filtration and ion exchange chromatography. These hemoproteins possess NADPH dependent O(2)(-)-producing and ferrihemoglobin-reducing activities. The incubation of neuropeptide PRP-1 (5 μg) with cytochrome b(558), caused elevation of these activities. The gel filtration results indicated possible binding of PRP-1 to these cytochromes b(558). PRP-1 activated both NADPH dependent O(2)(-)-producing and ferriHb-reducing activities of the cyt b(1)(558) and cyt b(2)(558), obtained from human lymphosarcoma tissue cells. One can assume that PRP-1 associated with cyt b(558) on the surface of the tumor cells by increasing both NADPH dependent O(2)(-)-producing and ferriHb-reducing activities of cyt b(558), increases the oxidation- reduction status. Changing the oxidation-reduction status and oxygen homeostasis of the tumor cells by PRP-1 can serve as one of the possible explanation of antitumorigenic effect of this cytokine.

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Curcumin dramatically enhances retinoic acid-induced superoxide generating activity via accumulation of p47-phox and p67-phox proteins in U937 cells

Cited by 22 publications

References 24 publications

Curcumin Stimulates Reactive Oxygen Species Production and Potentiates Apoptosis Induction by the Antitumor Drugs Arsenic Trioxide and Lonidamine in Human Myeloid Leukemia Cell Lines

Curcumin Stimulates Reactive Oxygen Species Production and Potentiates Apoptosis Induction by the Antitumor Drugs Arsenic Trioxide and Lonidamine in Human Myeloid Leukemia Cell Lines

GCN5 Regulates the Superoxide-Generating System in Leukocytes Via Controlling gp91-phox Gene Expression

Proline Rich Polypeptide (PRP-1) Increases the Superoxide-Producing and Ferrihemoglobin Reducing Activities of Cytochrome B558 Isoforms from Human Lymphosarcoma Tissue Cells

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