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[Cancer Research 47, 1302-1307, March 1, 1987]
© 1987 American Association for Cancer Research

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Differential Effects of Various Protein Kinase C Activators on Protein Phosphorylation in Human Acute Myeloblastic Leukemia Cell Line KG-1 and Its Phorbol Ester-resistant Subline KG-1a1

Zoltan Kiss, Eva Deli, Mamoru Shoji, H. Phillip Koeffler2, George R. Pettit, William R. Vogler and J. F. Kuo

Departments of Pharmacology [Z. K., E. D., J. F. K.] and Medicine (Hematology and Oncology) [M. S., W. R. V.], Emory University School of Medicine, Atlanta, Georgia 30322; Department of Medicine (Hematology/Oncology) [H. P. K.], University of California at Los Angeles, Los Angeles, California 90024; and Cancer Research Institute and Department of Chemistry [G. R. P.], Arizona State University, Tempe, Arizona 85287

Human myeloid leukemia KG-1 cells are induced to differentiate to macrophage-like cells by tumor-promoting phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Cells from the cloned subline, KG-1a, unlike the parental line, are resistant to the differentiating effect of TPA. In the present studies, we investigated in these cells protein phosphorylation stimulated by various protein kinase C activators, including 1-oleoyl-2-acetylglycerol in the presence of the diacylglycerol kinase inhibitor R59022, TPA, mezerein, and bryostatin. All the agents stimulated, to a greater extent and with a higher potency, phosphorylation of several proteins in KG-1 cells than in KG-1a cells. On the other hand, these agents markedly stimulated phosphorylation of other proteins in KG-1a cells compared to that in KG-1 cells. The findings indicated that the actions of the diacylglycerol, 1-oleoyl-2-acetylglycerol, and the non-metabolizable activators (TPA, mezerein, and bryostatin) were very similar but not fully equivalent; and that KG-1a cells exhibited altered (increased or decreased) phosphorylation patterns, perhaps related to the TPA resistance characteristic of this subline of cells.

1 Supported by USPHS Research Grants CA-36777, HL-15696, and NS-17608 (J. F. K.), CA-26038 and CA-32737 (H. P. K.), CA-29850 (W. R. V.), and CA-16094 and N01-CM-97262 (G. R. P.).

2 Recipient of USPHS Research Career Development Award and a member of Johnson Cancer Center.

Received 7/30/86. Revised 11/13/86. Accepted 12/ 1/86.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1987 by the American Association for Cancer Research.