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Cell Growth & Differentiation, Vol 6, Issue 10 1199-1205, Copyright © 1995 by American Association of Cancer Research
ARTICLES |
D Agrawal, F Dong, YZ Wang, D Kayda and WJ Pledger
H. Lee Moffitt Cancer Center and Research Institute, University of South Florida College of Medicine, Tampa 33612, USA.
We have examined the level of cyclin E, a G1 cyclin, and p27kip, a cyclin-dependent kinase inhibitor, in BALB/c 3T3 cells. Cell populations stimulated to undergo cell cycle traverse displayed little change in the level of cyclin E, while p27kip was found to be reduced 50-80% in proliferating cells. Analysis of mitotic cells, however, revealed that cyclin E is virtually absent and begins to reaccumulate soon after mitosis is complete, as does p27kip. Immunoprecipitation experiments revealed that p27kip is associated with cyclin E in quiescent but not proliferating cells, indicating that it may function to prevent development of cyclin E activity in the absence of growth factors. Based on our characterization of cyclin E and p27kip in BALB/c 3T3 cells during progression of the cell cycle, we propose a model of growth regulation controlling the G1 phase of growing and quiescent cells involving mitotic degradation of cyclin E and recovery of p27kip inhibitory activity in a late or postmitotic interval.
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