The G1-phase growth-arresting action of interleukin-1 is independent of p53 and p21/WAF1 function - PubMed (original) (raw)
. 1998 Nov 13;273(46):30517-23.
doi: 10.1074/jbc.273.46.30517.
Affiliations
- PMID: 9804820
- DOI: 10.1074/jbc.273.46.30517
Free article
The G1-phase growth-arresting action of interleukin-1 is independent of p53 and p21/WAF1 function
A Nalca et al. J Biol Chem. 1998.
Free article
Abstract
Interleukin-1 (IL-1) causes G1-phase growth arrest of A375-C6 human melanoma cells by hypophosphorylation of the retinoblastoma susceptibility gene product Rb. Because p53 and p21/WAF1 proteins are key components of growth arrest pathways involving Rb hypophosphorylation, we tested the functional role of these two proteins in IL-1 action. Exposure to IL-1 caused induction of both p53 and p21/WAF1 proteins. However, inhibition of p53 function by the K1 mutant of SV40-T antigen or by m175 (Arg to His) dominant-negative mutant of p53 did not result in abrogation of IL-1 action, suggesting that p53 function is not required for growth arrest by IL-1. Studies aimed at testing the role of p21/WAF1 in IL-1 action indicated that IL-1 induced p21/WAF1 expression independently of the p53 status of the cells. However, inhibition of p21/WAF1 expression resulted in only a marginal rescue from the growth-arresting action of IL-1. These findings imply that despite their induction, neither wild-type p53 nor p21 can fully account for the growth arrest by IL-1. Thus, a p53- and p21-independent pathway(s) mediates IL-1 action.
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