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Titolo:
IGF-I receptor signaling in a prostatic cancer cell line with a PTEN mutation
Autore:
Reiss, K; Wang, JY; Romano, G; Furnari, FB; Cavenee, WK; Morrione, A; Tu, X; Baserga, R;
Indirizzi:
Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA Ludwig Inst Canc Res, La Jolla, CA 92093 USA Ludwig Inst Canc Res La Jolla CA USA 92093 nc Res, La Jolla, CA 92093 USA
Titolo Testata:
ONCOGENE
fascicolo: 22, volume: 19, anno: 2000,
pagine: 2687 - 2694
SICI:
0950-9232(20000518)19:22<2687:IRSIAP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-I; DOMINANT-NEGATIVE MUTANT; FOCAL ADHESION KINASE; SMOOTH-MUSCLE CELLS; INSULIN-RECEPTOR; TUMOR-GROWTH; INSULIN-LIKE-GROWTH-FACTOR-1 RECEPTOR; TYROSINE PHOSPHORYLATION; ALPHA-V-BETA-3 INTEGRIN; BINDING-PROTEINS;
Keywords:
insulin-like growth factor; IGF-I receptor; prostate cancer; PTEN; IRS-I;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Baserga, R Thomas Jefferson Univ, Kimmel Canc Ctr, 233 S 10th St,624 BLSB,Philadelphia, PA 19107 USA Thomas Jefferson Univ 233 S 10th St,624 BLSB Philadelphia PA USA 19107
Citazione:
K. Reiss et al., "IGF-I receptor signaling in a prostatic cancer cell line with a PTEN mutation", ONCOGENE, 19(22), 2000, pp. 2687-2694

Abstract

LNCaP prostatic cancer cells are characterized by having a PTEN mutation, low levels of type 1 insulin-like growth factor receptor (IGF-IR) and no IRS-1, one of the major substrates of the IGF-IR, The absence of IRS-1, an activator of PI3-kinase, is compensated in these cells by the mutation in PTEN, an inhibitor of PI3-kinase, However, IGF-IR signaling in the absence of IRS-1 can cause cell differentiation and growth arrest. We hypothesized that these three characteristics may not be unrelated, specifically that, together, they may favor the metastatic spread of prostatic cancer cells without decreasing their growth potential. In support of this hypothesis, we report here that: (1) IRS-1 expression increases cell adhesion and decreases cell motility; (2) over-expression of the IGF-IR, in the absence of IRS-1, causes growth arrest and (3) a combination of TGF-IR and IRS-1 restores the transformed phenotype of LNCaP cells. These findings suggest a mechanism by which prostatic cancer cells can achieve metastatic potential without interfering with their growth potential.

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Documento generato il 05/12/20 alle ore 13:46:11