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Titolo:
Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1
Autore:
Wulf, GM; Ryo, A; Wulf, GG; Lee, SW; Niu, TH; Petkova, V; Lu, KP;
Indirizzi:
Harvard Univ, Sch Med, Div Hematol & Oncol, Canc Biol Program, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Canc Biol Program, Boston, MA 02115 USA Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA02115 USA Harvard Univ Boston MA USA 02115 s Med Ctr, Dept Med, Boston, MA02115 USA Harvard Univ, Sch Publ Hlth, Program Populat Genet, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 gram Populat Genet, Boston, MA 02115 USA Univ Gottingen, Tumorzentrum Goettingen, Dept Hematol & Oncol, D-3400 Gottingen, Germany Univ Gottingen Gottingen Germany D-3400 Oncol, D-3400 Gottingen, Germany
Titolo Testata:
EMBO JOURNAL
fascicolo: 13, volume: 20, anno: 2001,
pagine: 3459 - 3472
SICI:
0261-4189(20010702)20:13<3459:PIOIBC>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROLINE ISOMERIZATION; PEPTIDYL-PROLYL ISOMERASE; SKIN TUMOR-DEVELOPMENT; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; HA-RAS; SUBSTRATE RECOGNITION; CIS/TRANS ISOMERASES; REGULATORY MECHANISM; FUNCTIONAL-ANALYSIS;
Keywords:
cancer; c-Jun; cyclin D1; Pin1; Ras signaling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Lu, KP Harvard Univ, Sch Med, Div Hematol & Oncol, Canc Biol Program, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 iol Program, Boston, MA 02115 USA
Citazione:
G.M. Wulf et al., "Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1", EMBO J, 20(13), 2001, pp. 3459-3472

Abstract

Phosphorylation on serines or threonines preceding proline (Ser/Thr-Pro) is a major signaling mechanism. The conformation of a subset of phosphorylated Ser/Thr-Pro motifs is regulated by the prolyl isomerase Pin1, Inhibitionof Pin1 induces apoptosis and may also contribute to neuronal death in Alzheimer's disease. However, little is known about the role of Pin1 in canceror in modulating transcription factor activity. Here we report that Pin1 is strikingly overexpressed in human breast cancers, and that its levels correlate with cyclin D1 levels in tumors. Overexpression of Pin1 increases cellular cyclin D1 protein and activates its promoter. Furthermore, Pin1 binds c-Jun that is phosphorylated on Ser63/73-Pro motifs by activated JNK or oncogenic Ras, Moreover, Pin1 cooperates with either activated Ras or JNK toincrease transcriptional activity of c-Jun towards the cyclin D1 promoter. Thus, Pin1 is up-regulated in human tumors and cooperates with Ras signaling in increasing c-Jun transcriptional activity towards cyclin D1, Given the crucial roles of Ras signaling and cyclin D1 overexpression in oncogenesis, our results suggest that overexpression of Pin1 may promote tumor growth.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 13:12:44