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Cyclin E, a redundant cyclin in breast cancer.

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Cyclin E, a redundant cyclin in breast cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Decaprio, J. A. Zalvide, J. Gray-bablin, J. Keyomarsi, K. Knickerbocker, C. J. Fox, M. P.
Description	Author Affiliation: Gray-Bablin J ( Division of Molecular Medicine, Wadsworth Center, Albany, NY 12201, USA.);
Abstract	Cyclin E is an important regulator of cell cycle progression that together with cyclin-dependent kinase (cdk) 2 is crucial for the G1/S transition during the mammalian cell cycle. Previously, we showed that severe overexpression of cyclin E protein in tumor cells and tissues results in the appearance of lower molecular weight isoforms of cyclin E, which together with cdk2 can form a kinase complex active throughout the cell cycle. In this study, we report that one of the substrates of this constitutively active cyclin E/cdk2 complex is retinoblastoma susceptibility gene product (pRb) in populations of breast cancer cells and tissues that also overexpress p16. In these tumor cells and tissues, we show that the expression of p16 and pRb is not mutually exclusive. Overexpression of p16 in these cells results in sequestering of cdk4 and cdk6, rendering cyclin D1/cdk complexes inactive. However, pRb appears to be phosphorylated throughout the cell cycle following an initial lag, revealing a time course similar to phosphorylation of glutathione S-transferase retinoblastoma by cyclin E immunoprecipitates prepared from these synchronized cells. Hence, cyclin E kinase complexes can function redundantly and replace the loss of cyclin D-dependent kinase complexes that functionally inactivate pRb. In addition, the constitutively overexpressed cyclin E is also the predominant cyclin found in p107/E2F complexes throughout the tumor, but not the normal, cell cycle. These observations suggest that overexpression of cyclin E in tumor cells, which also overexpress p16, can bypass the cyclin D/cdk4-cdk6/p16/pRb feedback loop, providing yet another mechanism by which tumors can gain a growth advantage.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	26
Volume Number	93
Language	English
Publisher	National Academy of Sciences
Publisher Date	1996-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Breast Neoplasms Pathology Cell Cycle Cyclins Physiology Proto-Oncogene Proteins Animals Physiopathology Cell Line Cyclin D1 Cyclin-Dependent Kinase 4 Cyclin-Dependent Kinases Biosynthesis Metabolism G1 Phase Mammals Mitotic Index Oncogene Proteins Ploidies Retinoblastoma Protein S Phase Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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