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Cell Growth & Differentiation Vol. 11, 501-506, September 2000
© 2000 American Association for Cancer Research


Articles

K562 Cells Resistant to Phorbol 12-Myristate 13-acetate-induced Growth Arrest: Dissociation of Mitogen-activated Protein Kinase Activation and Egr-1 Expression from Megakaryocyte Differentiation1

Candace Shelly, Lilli Petruzzelli and Roman Herrera2

Department of Cell Biology, Parke-Davis Pharmaceutical Research Division of Warner-Lambert Company, Ann Arbor, Michigan 48105 [C. S., R. H.], and Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan and Veteran’s Affairs Medical Center, Ann Arbor, Michigan 48109 [L. P.]

Abstract

The K562 cell line undergoes megakaryocytic differentiation in response to phorbol 12-myristate 13-acetate (PMA) stimulation. This event correlates with mitogen-activated protein kinase activation, cell cycle arrest, and expression of the Egr-1 transcription factor. We have isolated K562 cells that are resistant to the growth-inhibitory action of PMA. Molecular characterization demonstrates that PMA resistance is downstream from PMA-induced activation of the mitogen-activated protein kinase pathway. Although the levels of Egr-1 expression and cyclic AMP-responsive element-binding protein phosphorylation are comparable in wild-type and PMA-resistant clones in response to PMA, the expression of megakaryocytic cell surface marker CD41 is detected only in the wild-type cells. The lack of differentiation of the PMA-resistant clones correlates with a failure of the PMA-treated cells to induce dephosphorylation and down-regulation of the retinoblastoma protein. These cells may provide a useful model system to distinguish those events that are connected to cell cycle arrest from those involved in the differentiation program initiated by PMA.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2000 by the American Association of Cancer Research.