CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Molla, A.
Right arrow Articles by Block, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Molla, A.
Right arrow Articles by Block, M. R.
Cell Growth & Differentiation Vol. 11, 83-90, February 2000
© 2000 American Association for Cancer Research


Articles

Adherence of Human Erythroleukemia Cells Inhibits Proliferation without Inducing Differentiation1

Annie Molla2 and Marc R. Block

Laboratoire d’étude de la différenciation et de l’adhérence cellulaires, UMR Centre National de la Recherche Scientifique/UJF 5538, Institut Albert Bonniot, Faculté de Médecine Domaine de la Merci, 38706 La Tronche Cedex, France

Abstract

To investigate the effect of extracellular matrix molecules in the megakaryocytic lineage, we studied the role of integrin engagement in the proliferation and differentiation of human erythroleukemia (HEL) cells. HEL cells grew in suspension, but their adherence depended upon the presence of matrix proteins or protein kinase C signaling. Adherence by itself did not trigger commitment of these cells but accelerated phorbol 12-myristate 13-acetate-induced differentiation. HEL cells adhered to fibronectin mainly through {alpha}5ß1, and this receptor acted synergetically with {alpha}4ß1. Integrin engagement induced cell growth arrest through mitogen-activated protein kinase inactivation. Such down-regulation of the mitogen-activated protein kinase pathway by integrin engagement was suggested as a megakaryocytic-platelet lineage specificity. This signaling was not restricted to a peculiar integrin but was proposed as a general mechanism in these cells.




This article has been cited by other articles:


Home page
J Biol ChemHome page
Y. Saito, T. Owaki, T. Matsunaga, M. Saze, S. Miura, M. Maeda, M. Eguchi, R. Tanaka, J. Taira, H. Kodama, et al.
Apoptotic Death of Hematopoietic Tumor Cells through Potentiated and Sustained Adhesion to Fibronectin via VLA-4
J. Biol. Chem., March 5, 2010; 285(10): 7006 - 7015.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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.