AustralieFrV1, Main, Exploration, bibRecord, 00AF83

p27Kip1 induces quiescence and growth factor insensitivity in tamoxifen-treated breast cancer cells

Identifieur interne : 00AF83 ( Main/Exploration ); précédent : 00AF82; suivant : 00AF84

p27Kip1 induces quiescence and growth factor insensitivity in tamoxifen-treated breast cancer cells

Auteurs : Jason S. Carroll [Australie] ; Danielle K. Lynch [Australie] ; Alexander Swarbrick [Australie] ; Jack-Michel Renoir [France] ; Boris Sarcevic [Australie] ; Roger J. Daly [Australie] ; Elizabeth A. Musgrove [Australie] ; Robert L. Sutherland [Australie]

Source :

Cancer research : (Baltimore) [ 0008-5472 ] ; 2003.

RBID : Pascal:04-0117647

Descripteurs français

Pascal (Inist)
- Tamoxifène, Homme, In vitro, Cellule tumorale, Tumeur maligne, Glande mammaire, Résistance, Activité biologique, Anticancéreux, Expression génique, Gène suppresseur tumeur, Mécanisme action, Multiplication cellulaire, Quiescence, Sensibilité résistance, Facteur croissance, Gène p27.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Antineoplastic agent, Biological activity, Cell proliferation, Gene expression, Growth factor, Human, In vitro, Malignant tumor, Mammary gland, Mechanism of action, Quiescence, Resistance, Sensitivity resistance, Tamoxifene, Tumor cell, Tumor suppressor gene.

Abstract

Tamoxifen, a selective estrogen-receptor modulator, is effective in the treatment and prevention of breast cancer, but therapeutic resistance is common. Pure steroidal antiestrogens are efficacious in tamoxifen-resistant disease and, unlike tamoxifen, arrest cells in a state of quiescence from which they cannot reenter the cell cycle after growth factor stimulation. We now show that in hydroxytamoxifen-treated cells, transduction of the cell cycle inhibitor p27^Kip1 induces quiescence and insensitivity to growth stimulation by insulin/insulin-like growth factor I and epidermal growth factor/transforming growth factor a. Furthermore, reinitiation of cell cycle progression by insulin/insulin-like growth factor I in hydroxytamoxifen-arrested cells involves dissociation of the corepressors nuclear receptor corepressor (N-CoR) and silencing mediator for retinoid and thyroid hormone receptor (SMRT) from nuclear estrogen receptor a and redistribution to the cytoplasm, a process that is inhibited by mitogen-activated proteinlextracellular signal-regulated kinase, but not phosphatidylinositol 3'-kinase, inhibitors. These data suggest that agents that up-regulate p27^Kip1or inhibit growth factor signaling via the extracellular signal-regulated kinases should be tested as therapeutic strategies in tamoxifen-resistant breast cancer.

Affiliations:

Australie, France

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Tamoxifen, a selective estrogen-receptor modulator, is effective in the treatment and prevention of breast cancer, but therapeutic resistance is common. Pure steroidal antiestrogens are efficacious in tamoxifen-resistant disease and, unlike tamoxifen, arrest cells in a state of quiescence from which they cannot reenter the cell cycle after growth factor stimulation. We now show that in hydroxytamoxifen-treated cells, transduction of the cell cycle inhibitor p27<sup>Kip1</sup>
 induces quiescence and insensitivity to growth stimulation by insulin/insulin-like growth factor I and epidermal growth factor/transforming growth factor a. Furthermore, reinitiation of cell cycle progression by insulin/insulin-like growth factor I in hydroxytamoxifen-arrested cells involves dissociation of the corepressors nuclear receptor corepressor (N-CoR) and silencing mediator for retinoid and thyroid hormone receptor (SMRT) from nuclear estrogen receptor a and redistribution to the cytoplasm, a process that is inhibited by mitogen-activated proteinlextracellular signal-regulated kinase, but not phosphatidylinositol 3'-kinase, inhibitors. These data suggest that agents that up-regulate p27<sup>Kip1</sup>
or inhibit growth factor signaling via the extracellular signal-regulated kinases should be tested as therapeutic strategies in tamoxifen-resistant breast cancer.</div>
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p27Kip1 induces quiescence and growth factor insensitivity in tamoxifen-treated breast cancer cells

p27Kip1 induces quiescence and growth factor insensitivity in tamoxifen-treated breast cancer cells

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri