Effects of a novel synthetic retinoid on malignant glioma in vitro : inhibition of cell proliferation, induction of apoptosis and differentiation
Identifieur interne : 003601 ( Main/Exploration ); précédent : 003600; suivant : 003602Effects of a novel synthetic retinoid on malignant glioma in vitro : inhibition of cell proliferation, induction of apoptosis and differentiation
Auteurs : S. L Costa [France] ; E. Paillaud [France] ; C. Fages [France] ; C. Rochette-Egly [France] ; J. L Plassat [France] ; H. Jouault [France] ; A. Perzelova [Slovaquie] ; M. Tardy [France]Source :
- European Journal of Cancer [ 0959-8049 ] ; 2001.
Abstract
Among six synthetic retinoids tested, the retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) was highly efficient in inducing growth inhibition of 8MG-BA and GL-15 human glioblastoma cell lines, with growth arrest at the S phase of the cell cycle. CD 437 also induced apoptosis in these cells, with 8MG-BA being the most sensitive. In these cells, induction of apoptosis by CD437 has been related to the downregulation of Bcl-2 expression and to CPP32 activation, but not to p53 expression. The remaining non-apoptotic cells presented a morphological pattern of astroglial differentiation with overexpression of glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS). The mechanism of action of CD437, originally developed as a RARγ agonist, is not yet elucidated. However, our results suggest that it acts through an increase of the expression of retinoid-inducible genes, such as RARβ2 and/or RARα2.
Url:
DOI: 10.1016/S0959-8049(00)00430-5
Affiliations:
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CD 437 also induced apoptosis in these cells, with 8MG-BA being the most sensitive. In these cells, induction of apoptosis by CD437 has been related to the downregulation of Bcl-2 expression and to CPP32 activation, but not to p53 expression. The remaining non-apoptotic cells presented a morphological pattern of astroglial differentiation with overexpression of glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS). The mechanism of action of CD437, originally developed as a RARγ agonist, is not yet elucidated. However, our results suggest that it acts through an increase of the expression of retinoid-inducible genes, such as RARβ2 and/or RARα2.</div></front></TEI><affiliations><list><country><li>France</li><li>Slovaquie</li></country><region><li>Île-de-France</li></region><settlement><li>Créteil</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Costa, S L" sort="Costa, S L" uniqKey="Costa S" first="S. L" last="Costa">S. 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Perzelova</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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