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| Constitutive overexpression of cyclin D-1 in human breast epithelial cells does not prevent G(1) arrest induced by deprivation of epidermal growth factor |
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| Author(s): Chou JL, Fan Z, DeBlasio T, Koff A, Rosen N, Mendelsohn J |
| Source: BREAST CANCER RESEARCH AND TREATMENT Volume: 55 Issue: 3 Pages: 267-283 Published: JUN 1999 |
| Times Cited: 28 References: 72 |
| Abstract: Non-transformed human breast epithelial cell line MCF10A is dependent on exogenous epidermal growth factor (EGF) for continued growth. Complete G(1) arrest was rapidly induced following EGF deprivation. The cell cycle arrest was accompanied by increased levels of p27(KIP1), a cyclin-dependent kinase inhibitor, and reduced level of cyclin D-1. This was associated with strong inhibition of cyclin-dependent kinase 2 and cyclin D-1-associated kinase activities. Introduction of exogenous cyclin D-1 into MCF10A (MCF10AD1) cells resulted in an accelerated cell growth rate but did not confer colony-forming capacity. Cell cycle arrest was still achieved in MCF10AD1 cells following EGF deprivation. In the great majority of MCF10AD1 clones, accumulation in G(1) phase was accompanied by reduced cyclin D-1 and increased p27(KIP1) protein levels. In two clones where cyclin D-1 remained unchanged during G(1) arrest, it was found that more cyclin D-1 protein was bound to p27(KIP1). The data demonstrate that ectopic expression of cyclin D-1 alone could not transform MCF10A cells nor was it sufficient to prevent G(1) arrest induced by EGF deprivation. |
| Document Type: Article |
| Language: English |
| Reprint Address: Chou, JL (reprint author), Mem Sloan Kettering Canc Ctr, 1275 York Ave,Box 481, New York, NY 10021 USA |
Addresses:
1. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA 2. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA |
| Publisher: KLUWER ACADEMIC PUBL, SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS |
| Subject Category: Oncology |
| IDS Number: 230VH |
| ISSN: 0167-6806 |
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| |  |  |  |  | | | | Record from Web of Science® | |  |  | | | | | | |