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IL-1によるp21^WAF1の発現の意義：大沢宜明^１,2、蜂谷みさを^１、明石真言^１（¹放医研・放障医, ²東大・医・放健）

p21^WAF1 accumulation without cell cycle arrest by IL-1 in human embryonic fibroblasts : Yoshiaki OSAWA^1,2, Misao HACHIYA¹, and Makoto AKASHI¹ (¹Div.of Rad. Health, Natl. Inst. Radiol. Sci., ²Dept. of Radiol. Health, Fac. of Med., Univ. of Tokyo)

Cell cycle progression is controlled by extra- and intra-cellular signals. Interleukin-1 (IL-1) stimulates various types of cells; IL-1 also has an anti-proliferative effect on both tumor and normal cells of certain tissues. WI38 human embryonic fibro-blasts produce IL-1 and IL-1 induces p21^WAF1 expression though a p53-independent pathway in these cells. However, IL-1 did not cause the cell cycle-arrest. In order to explore the mechanisms, yclin-dependent kinase 2 (cdk2) was immunoprecipitated. Western blot analysis showed that levels of p21^WAF1 in cdk2 immunoprecipipate were increased by IL-1. How-ever, kinase assays of cdk2 immunoprecipitate using histone H1 as a substrate found that IL-1 failed to reduce the kinase activity, and IL-1 did not increase levels of hypophos-phorylated retinoblastoma gene product (Rb). We also determined levels of other cell cycle-associated proteins, cdk2, cdk4, cyclin D1, cyclin E, and a cdk2 inhibitor, p27. IL-1 decreased the accumulation of p27 protein as compared to that in untreated cells while there were no effects of IL-1 on levels of other proteins determined. The mecha-nisms for lacking of growth inhibition remain unknown. The p27 protein level may be critical for the cell cycle arrest in these cells. Further studies are in progress.