AustralieFrV1, PascalFrancis, Curation, bibRecord, 000F57

Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells

Identifieur interne : 000F57 ( PascalFrancis/Curation ); précédent : 000F56; suivant : 000F58

Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells

Auteurs : Sophie F. Doisneau-Sixou [France, Australie] ; Philippe Cestac [France] ; Sarah Chouini [France] ; Jason S. Carroll [France, Australie] ; Andrew D. Hamilton [États-Unis] ; Said M. Sebti [États-Unis] ; Marc Poirot [France] ; Patrick Balaguer [France] ; Jean-Charles Faye [France] ; Robert L. Sutherland [Australie] ; Gilles Favre [France]

Source :

Endocrinology : (Philadelphia) [ 0013-7227 ] ; 2003.

RBID : Pascal:03-0470950

Abstract

Activation of estrogen receptors (ERs) by estrogens triggers both ER nuclear transcriptional activity and Src/Ras/Erks pathway-dependent mitogenic activity. The present study implicates prenylated proteins in both estrogenic actions. The farnesyltransferase and geranylgeranyltransferase I inhibitors (FTI-277 and GGTI-298, respectively) antagonize estradiol-stimulated cell cycle progression, progesterone receptor, cyclin D1, and c-Myc expression. In contrast, the inhibitors markedly stimulate transcription from two genes containing estrogen response elements, both in the absence and presence of estradiol. The pure antiestrogen ICI 182,780 inhibits by more than 85% these effects on transcription. We demonstrate that both FTI-277 and GGTI-298 increase the association of steroid receptor coactivator-1 with ERa and FTI-277 decreases the association of ERa with the histone deacetylase 1, a known transcriptional repressor. In addition, FTI-277 has no marked effect on the association of the two corepressors, nuclear receptor corepressor and silencing mediator of retinoid and thyroid receptor with ERa, whereas GGTI-298, similar to tamoxifen, clearly increased these associations. Together, these results demonstrate that prenylated proteins play a role in estradiol stimulation of proliferation and progesterone receptor expression. However, they antagonize the ability of ERa to stimulate estrogen response element-dependent transcriptional activity, acting presumably through coregulator complex formation.

A01	`01`	`1`		`@0 0013-7227`
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A03		`1`		`@0 Endocrinology : (Phila.)`
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A08	`01`	`1`	`ENG`	`@1 Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells`
A11	`01`	`1`		`@1 DOISNEAU-SIXOU (Sophie F.)`
A11	`02`	`1`		`@1 CESTAC (Philippe)`
A11	`03`	`1`		`@1 CHOUINI (Sarah)`
A11	`04`	`1`		`@1 CARROLL (Jason S.)`
A11	`05`	`1`		`@1 HAMILTON (Andrew D.)`
A11	`06`	`1`		`@1 SEBTI (Said M.)`
A11	`07`	`1`		`@1 POIROT (Marc)`
A11	`08`	`1`		`@1 BALAGUER (Patrick)`
A11	`09`	`1`		`@1 FAYE (Jean-Charles)`
A11	`10`	`1`		`@1 SUTHERLAND (Robert L.)`
A11	`11`	`1`		`@1 FAVRE (Gilles)`
A14	`01`			`@1 Département "Innovation Thérapeutique et Oncologie Moléculaire", Centre de Physiopathologie de Toulouse Purpan, Institut National de la Santé et de la Recherche Médicale U563, and Institut Claudius Regaud @2 31052 Toulouse @3 FRA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 7 aut. @Z 9 aut. @Z 11 aut.`
A14	`02`			`@1 Cancer Research Program, Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst @2 Sydney, New South Wales 2010 @3 AUS @Z 1 aut. @Z 4 aut. @Z 10 aut.`
A14	`03`			`@1 Department of Chemistry, Yale University @2 New Haven, Connecticut 06511 @3 USA @Z 5 aut.`
A14	`04`			`@1 Drug Discovery Program, H. Lee Moffitt Cancer Center and Research Institute and Department of Biochemistry and Molecular Biology, University of South Florida @2 Tampa, Florida 33612 @3 USA @Z 6 aut.`
A14	`05`			`@1 Institut National de la Santé et de la Recherche Médicale 439, Pathologie Moléculaire des Récepteurs Nucléaires @2 34090 Montpellier @3 FRA @Z 8 aut.`
A20				`@1 989-998`
A21				`@1 2003`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 2086 @5 354000104289600280`
A44				`@0 0000 @1 © 2003 INIST-CNRS. All rights reserved.`
A45				`@0 64 ref.`
A47	`01`	`1`		`@0 03-0470950`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Endocrinology : (Philadelphia)`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Activation of estrogen receptors (ERs) by estrogens triggers both ER nuclear transcriptional activity and Src/Ras/Erks pathway-dependent mitogenic activity. The present study implicates prenylated proteins in both estrogenic actions. The farnesyltransferase and geranylgeranyltransferase I inhibitors (FTI-277 and GGTI-298, respectively) antagonize estradiol-stimulated cell cycle progression, progesterone receptor, cyclin D1, and c-Myc expression. In contrast, the inhibitors markedly stimulate transcription from two genes containing estrogen response elements, both in the absence and presence of estradiol. The pure antiestrogen ICI 182,780 inhibits by more than 85% these effects on transcription. We demonstrate that both FTI-277 and GGTI-298 increase the association of steroid receptor coactivator-1 with ERa and FTI-277 decreases the association of ERa with the histone deacetylase 1, a known transcriptional repressor. In addition, FTI-277 has no marked effect on the association of the two corepressors, nuclear receptor corepressor and silencing mediator of retinoid and thyroid receptor with ERa, whereas GGTI-298, similar to tamoxifen, clearly increased these associations. Together, these results demonstrate that prenylated proteins play a role in estradiol stimulation of proliferation and progesterone receptor expression. However, they antagonize the ability of ERa to stimulate estrogen response element-dependent transcriptional activity, acting presumably through coregulator complex formation.
C02	`01`	`X`		`@0 002A`
N21				`@1 321`
N82				`@1 DST`

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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells</title>
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<author><name sortKey="Hamilton, Andrew D" sort="Hamilton, Andrew D" uniqKey="Hamilton A" first="Andrew D." last="Hamilton">Andrew D. Hamilton</name>
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<author><name sortKey="Sebti, Said M" sort="Sebti, Said M" uniqKey="Sebti S" first="Said M." last="Sebti">Said M. Sebti</name>
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<author><name sortKey="Poirot, Marc" sort="Poirot, Marc" uniqKey="Poirot M" first="Marc" last="Poirot">Marc Poirot</name>
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<author><name sortKey="Balaguer, Patrick" sort="Balaguer, Patrick" uniqKey="Balaguer P" first="Patrick" last="Balaguer">Patrick Balaguer</name>
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<author><name sortKey="Faye, Jean Charles" sort="Faye, Jean Charles" uniqKey="Faye J" first="Jean-Charles" last="Faye">Jean-Charles Faye</name>
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<author><name sortKey="Sutherland, Robert L" sort="Sutherland, Robert L" uniqKey="Sutherland R" first="Robert L." last="Sutherland">Robert L. Sutherland</name>
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<author><name sortKey="Favre, Gilles" sort="Favre, Gilles" uniqKey="Favre G" first="Gilles" last="Favre">Gilles Favre</name>
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<series><title level="j" type="main">Endocrinology : (Philadelphia)</title>
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<front><div type="abstract" xml:lang="en">Activation of estrogen receptors (ERs) by estrogens triggers both ER nuclear transcriptional activity and Src/Ras/Erks pathway-dependent mitogenic activity. The present study implicates prenylated proteins in both estrogenic actions. The farnesyltransferase and geranylgeranyltransferase I inhibitors (FTI-277 and GGTI-298, respectively) antagonize estradiol-stimulated cell cycle progression, progesterone receptor, cyclin D1, and c-Myc expression. In contrast, the inhibitors markedly stimulate transcription from two genes containing estrogen response elements, both in the absence and presence of estradiol. The pure antiestrogen ICI 182,780 inhibits by more than 85% these effects on transcription. We demonstrate that both FTI-277 and GGTI-298 increase the association of steroid receptor coactivator-1 with ERa and FTI-277 decreases the association of ERa with the histone deacetylase 1, a known transcriptional repressor. In addition, FTI-277 has no marked effect on the association of the two corepressors, nuclear receptor corepressor and silencing mediator of retinoid and thyroid receptor with ERa, whereas GGTI-298, similar to tamoxifen, clearly increased these associations. Together, these results demonstrate that prenylated proteins play a role in estradiol stimulation of proliferation and progesterone receptor expression. However, they antagonize the ability of ERa to stimulate estrogen response element-dependent transcriptional activity, acting presumably through coregulator complex formation.</div>
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Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells

Contrasting effects of prenyltransferase inhibitors on estrogen-dependent cell cycle progression and estrogen receptor-mediated transcriptional activity in MCF-7 cells

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