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Titolo:
HER4 mediates ligand-dependent antiproliferative and differentiation responses in human breast cancer cells
Autore:
Sartor, CI; Zhou, H; Kozlowska, E; Guttridge, K; Kawata, E; Caskey, L; Harrelson, J; Hynes, N; Ethier, S; Calvo, B; Earp, HS;
Indirizzi:
Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 Oncol, Chapel Hill, NC 27599 USA Univ N Carolina, Dept Surg, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 Surg, Chapel Hill, NC 27599 USA Univ N Carolina, Dept Internal Med & Pharmacol, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 macol, Chapel Hill, NC 27599 USA Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USAUniv N Carolina Chapel Hill NC USA 27599 c Ctr, Chapel Hill, NC 27599 USA Friedrich Miescher Inst, CH-4002 Basel, Switzerland Friedrich Miescher Inst Basel Switzerland CH-4002 002 Basel, Switzerland Univ Michigan, Dept Radiat Oncol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 adiat Oncol, Ann Arbor, MI 48109 USA
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 13, volume: 21, anno: 2001,
pagine: 4265 - 4275
SICI:
0270-7306(200107)21:13<4265:HMLAAD>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPIDERMAL GROWTH-FACTOR; FACTOR RECEPTOR; SIGNAL-TRANSDUCTION; TUMOR-CELLS; TYROSINE PHOSPHORYLATION; RETROVIRAL VECTORS; DOWN-REGULATION; ERBB RECEPTORS; NEU; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Sartor, CI Univ N Carolina, Dept Radiat Oncol, Campus Box 7512, Chapel Hill, NC 27599USA Univ N Carolina Campus Box 7512 Chapel Hill NC USA 27599 599USA
Citazione:
C.I. Sartor et al., "HER4 mediates ligand-dependent antiproliferative and differentiation responses in human breast cancer cells", MOL CELL B, 21(13), 2001, pp. 4265-4275

Abstract

The function of the epidermal growth factor receptor (EGFR) family member HER4 remains unclear because its activating ligand, heregulin, results in either proliferation or differentiation. This variable response may stem from the range of signals generated by HER4 homodimers versus heterodimeric complexes with other EGFR family members. The ratio of homo- and heterodimeric complexes may be influenced both by a cell's EGFR family member expression profile and by the ligand or even ligand isoform used. To define the roleof HER4 in mediating antiproliferative and differentiation responses, human breast cancer cell lines were screened for responses to heregulin. Only cells that expressed HER4 exhibited heregulin-dependent antiproliferative responses. In-depth studies of one line, SUM44, demonstrated that the antiproliferative and differentiation responses correlated with HER4 activation and were abolished by stable expression of a kinase-inactive HER4. HB-EGF, a HER4-specific ligand in this EGFR-negative cell line, also induced an antiproliferative response. Moreover, introduction and stable expression of HER4in HER4-negative SUM102 cells resulted in the acquisition of a heregulin-dependent antiproliferative response, associated with increases in markers of differentiation. The role of HER2 in these heregulin-dependent responses was examined through elimination of cell surface HER2 signaling by stable expression of a single-chain anti-HER2 antibody that sequestered HER2 in theendoplasmic reticulum. In the cell lines with either endogenously (SUM44) or exogenously (SUM102) expressed HER4, elimination of HER2 did not alter HER4-dependent decreases in cell growth. These results suggest that HER4 is both necessary and sufficient to trigger an antiproliferative response in human breast cancer cells.

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Documento generato il 29/11/20 alle ore 15:29:32