DI-UMONS : Dépôt institutionnel de l’université de Mons

Recherche transversale
(titres de publication, de périodique et noms de colloque inclus)
2007-08-01 - Article/Dans un journal avec peer-review - Anglais - 14 page(s)

Nonclercq Denis , Journé Fabrice, Laïos Ioanna, Chaboteaux Carole, Toillon Robert-Alain, Leclercq Guy, Laurent Guy , "Effect of nuclear export inhibition on estrogen receptor regulation in breast cancer cells" in Journal of Molecular Endocrinology, 39, 2, 105-118

  • Edition : Society for Endocrinology, Bristol (United Kingdom)
  • Codes CREF : Histologie (DI3212), Cancérologie (DI3349)
  • Unités de recherche UMONS : Histologie (M118)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
Texte intégral :

Abstract(s) :

(Anglais) We used the Crm1 inhibitor leptomycin B (LMB) to examine a possible involvement of nuclear export in estrogen receptor alpha (ER) level and function in MCF-7 breast carcinoma cells. As revealed by immunofluorescence microscopy and western blotting with anti-ER antibodies, LMB produced an accumulation of ER in cell nuclei. LMB also partly abrogated ER elimination resulting from Hsp90 disruption and 17beta-estradiol (E(2))-induced ER downregulation. By contrast, it was ineffective on ER downregulation caused by the pure anti-estrogen fulvestrant. Finally, LMB inhibited E(2)-induced progesterone receptor expression and the expression of an estrogen response element-driven luciferase reporter gene in unstimulated and E(2)-stimulated cells. Altogether, the data reported here suggest that: i) ER undergoes nuclear export directly or indirectly involving exportin Crm1; ii) degradation of unliganded and of agonist-bound ER probably occurs in an extranuclear compartment, while it is not the case for ER bound to a pure anti-estrogen; and iii) optimal ER-mediated gene transactivation seems to require nucleocytoplasmic shuttle of the receptor.

Identifiants :
  • PMID : 17693610
  • DOI : 10.1677/JME-07-0040