Information de reference pour ce titreAccession Number: | 00006374-200423250-00006.
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Author: | Knockaert, Marie 1; Blondel, Marc 1; Bach, Stephane 1; Leost, Maryse 1; Elbi, Cem 2; Hager, Gordon L 2; Nagy, Scott R 3; Han, Dalho 3; Denison, Michael 3; Ffrench, Martine 4; Ryan, Xiaozhou P 5; Magiatis, Prokopios 6; Polychronopoulos, Panos 6; Greengard, Paul 5; Skaltsounis, Leandros 6; Meijer, Laurent *,1,5
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Institution: | (1)C.N.R.S., Cell Cycle Group & UPS-2682, Station Biologique, BP 74, 29682 ROSCOFF cedex, Bretagne, France; (2)Laboratory of Receptor Biology & Gene Expression, Bldg 41, Room B602, National Cancer Institute, NIH, Bethesda, MD 20892-5055, USA; (3)Department of Environmental Toxicology, Meyer Hall, One Shields Avenue, University of California, Davis, CA 95616-8588, USA; (4)Universite Claude Bernard, Laboratoire de Cytologie Analytique et Cytogenetique Moleculaire, 8 Avenue Rockefeller, 69373 Lyon Cedex 08, France; (5)Laboratory of Molecular & Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA; (6)Division of Pharmacognosy and Natural Products Chemistry, Department of Pharmacy, University of Athens, Panepistimiopolis Zografou, GR-15771 Athens, Greece
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Title: | Independent actions on cyclin-dependent kinases and aryl hydrocarbon receptor mediate the antiproliferative effects of indirubins.[Article]
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Source: | Oncogene. 23(25):4400-4412, May 27, 2004.
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Abstract: | Indirubin, a bis-indole obtained from various natural sources, is responsible for the reported antileukemia activity of a Chinese Medicinal recipe, Danggui Longhui Wan. However, its molecular mechanism of action is still not well understood. In addition to inhibition of cyclin-dependent kinases and glycogen synthase kinase-3, indirubins have been reported to activate the aryl hydrocarbon receptor (AhR), a cotranscriptional factor. Here, we confirm the interaction of AhR and indirubin using a series of indirubin derivatives and show that their binding modes to AhR and to protein kinases are unrelated. As reported for other AhR ligands, binding of indirubins to AhR leads to its nuclear translocation. Furthermore, the apparent survival of AhR-/- and +/+ cells, as measured by the MTT assay, is equally sensitive to the kinase-inhibiting indirubins. Thus, the cytotoxic effects of indirubins are AhR-independent and more likely to be linked to protein kinase inhibition. In contrast, a dramatic cytostatic effect, as measured by actual cell counts and associated with a sharp G1 phase arrest, is induced by 1-methyl-indirubins, a subfamily of AhR-active but kinase-inactive indirubins. As shown for TCDD (dioxin), this effect appears to be mediated through the AhR-dependent expression of p27KIP1. Altogether these results suggest that AhR activation, rather than kinase inhibition, is responsible for the cytostatic effects of some indirubins. In contrast, kinase inhibition, rather than AhR activation, represents the main mechanism underlying the cytotoxic properties of this class of promising antitumor molecules.
Copyright (C) 2004 Nature Publishing Group
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Author Keywords: | aryl hydrocarbon receptor; indirubin; cyclin-dependent kinase; glycogen synthase kinase; GSK-3[beta]; kinase inhibitor; cancer.
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Language: | English.
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Document Type: | Original Papers.
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Journal Subset: | Clinical Medicine.
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ISSN: | 0950-9232
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NLM Journal Code: | onc, 8711562
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