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Titolo:
Increased expression of p27Kip1 arrests neuroblastoma cell growth
Autore:
Matsuo, T; Seth, P; Thiele, CJ;
Indirizzi:
NCI, Cell & Mol Sect, Pediat Oncol Branch, Div Clin Sci, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 ol Branch, Div Clin Sci, Bethesda, MD 20892 USA
Titolo Testata:
MEDICAL AND PEDIATRIC ONCOLOGY
fascicolo: 1, volume: 36, anno: 2001,
pagine: 97 - 99
SICI:
0098-1532(200101)36:1<97:IEOPAN>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
KINASE INHIBITOR P27(KIP1); HUMAN NEURO-BLASTOMA; DIFFERENTIATION; G(1); MYC; ACCUMULATION; LINE;
Keywords:
neuroblastoma; retinoids; cell cycle; p27Kip1; N-MYC; G(1) cyclin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Thiele, CJ NCI, Cell & Mol Sect, Pediat Oncol Branch, Div Clin Sci, 10 CtrDr,MSC-1928, Bethesda, MD 20892 USA NCI 10 Ctr Dr,MSC-1928 Bethesda MD USA20892 esda, MD 20892 USA
Citazione:
T. Matsuo et al., "Increased expression of p27Kip1 arrests neuroblastoma cell growth", MED PED ONC, 36(1), 2001, pp. 97-99

Abstract

Background and Procedure. To investigate the molecular mechanisms by whichretinoic acid (RA) alters cell growth, the expression and activity of components of the cell cycle machinery were analyzed. Results and Conclusions. Within 2 days of RA treatment, and prior to the arrest of NE cells in the G(1) phase of the cell cycle, there was a complete downregulation of Cl cyclin/cdk activities. Protein levels for the G(1) cyclin/cdk were essentially unchanged during this time, although there was a decrease in the steady-state levels of hyperphosphorylated Rb and p60N-MYC proteins. The cdk inhibitors, p21Cip1 and p27Kip1 were constitutively expressed in KCNR, while p15 INK4B and p16 INK4A mRNA were undetected. Within 24 hr of RA treatment, therewas a 4-fold increase in the expression of p27Kip1, although p27 mRNA levels were unchanged. Levels of p21Cip1 were unaltered. Coincident with the decreasein kinase activity there was an increase in p27 bound to G(1) cyclin/cdk. The increase in p21 was not due to an increase in transcription. In other cell systems, increased expression of c-MYC has been shown to lead to adecrease in p27 levels that is regulated at the post-transcriptional level(sequestration). To determine whether increased levels of N-MYC could affect the level of p27, we evaluated the expression of p27 in a series of N-MYC transfected cells and found that constitutive overexpression of N-MYC ledto a decrease in the steady-state levels of p27 and in p27 bound to G(1) cyclin/cdk complexes. Using adenoviral vectors expressing p27 we found that infection leads to increased p27 expression, which causes a decrease in cdkactivity and an accumulation of cells in G(1). Med. Pediatr. Oncol. 36: 97-99, 2001. Published 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 05:40:34