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Volume 271, Number 45, Issue of November 8, 1996 pp. 28469-28477
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Transcriptional Activation of the cdc2 Gene Is Associated with Fas-induced Apoptosis of Human Hematopoietic Cells

(Received for publication, January 29, 1996, and in revised form, June 14, 1996)

From the Division of Hemopoiesis, Institute of Hematology, and the Department of Hematology, Jichi Medical School, Tochigi 329-04, Japan, ^§ Katsuta Research Laboratory, Hitachi Koki Co., Ltd., Ibaraki 312, Japan, and ^¶ Tsukuba Research Institute, Banyu Pharmaceutical Co. Ltd., Ibaraki 300-33, Japan

Apoptosis has recently been hypothesized to be the result of aberrant cell cycle control. In this study, we have investigated the role of cell cycle-regulatory elements in Fas-induced apoptosis of hematopoietic cells. When HL-60 cells were treated with anti-Fas antibody, rapid activation of growth-associated histone H1 kinase was observed without any change in cell cycle distribution. This was accompanied by the increase in cdc2 mRNA expression and Cdc2 kinase activity. Up-regulation of cdc2 mRNA was similarly induced in BCL-2-overexpressing HL-60 subline by anti-Fas treatment independently of the appearance of apoptotic phenotypes. Fas-induced apoptosis was completely inhibited by butyrolactone I, a specific inhibitor of Cdc2 kinase. Moreover, the same phenomenon was observed during Fas-induced but not spontaneous apoptosis of postmitotic granulocytes. Finally, we have found that ``Fas-responsive element'' was located between nucleotides 730 and 552 of the cdc2 promoter and was responsive for transcriptional activation of the cdc2 gene during Fas-induced apoptosis. These results indicate that aberrant activation of Cdc2 is associated with Fas-induced apoptosis of hematopoietic cells, and that the mechanism of cdc2 transcription during Fas-induced apoptosis is different from that in normal cell cycle control.

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