p53 mediates density‐dependent growth arrest

FEBS Letters

Rotter, V.¹  Milyavsky, M.¹  Meerson, A.² 

[1] Department of Molecular Cell Biology, Weizmann Institute of Science, P.O. Box 26, Rehovot 76100, Israel;Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Hebrew University, Givat Ram, Jerusalem 91904, Israel

关键词: p53;    p16/INK4a;    Contact inhibition;    Density-dependent;   

DOI  :  10.1016/S0014-5793(04)00027-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

While the stress-response-associated importance of the p53 tumor suppressor is well established, recent studies have also linked p53 with several basic parameters in the normal behavior of cells. Here, we present evidence that basal p53 expression in WI38 human embryonic lung fibroblasts restricts growth rate and mediates density-dependent inhibition of growth and the associated G1 phase arrest of the cell cycle by affecting the density-dependent regulation of p16/INK4a. Additionally, we show that prolonged culturing of hTert-immortalized WI38 cells leads to a loss of density-dependent growth inhibition that correlates with p27/KIP deregulation as well as the previously shown INK4a locus silencing, and to an onset of contact-induced, p53-dependent cell death.

【 授权许可】

Unknown