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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Morena, A. Articles by Falcioni, R. Search for Related Content PubMed PubMed Citation Articles by Morena, A. Articles by Falcioni, R. Related Collections Hematopoiesis and Stem Cells Neoplasia Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2002, Vol. 100, No. 1, pp. 96-106 HEMATOPOIESIS Expression of the 4 integrin subunit induces monocytic differentiation of 32D/v-Abl cells Annarita Morena, Sabrina Riccioni, Alessandra Marchetti, Alessandro Tartaglia Polcini, Arthur M. Mercurio, Giovanni Blandino, Ada Sacchi, and Rita Falcioni From the Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, Via delle Messi d'Oro, Rome, Italy; and the Department of Pathology Research North, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA. The 64 integrin is the receptor for various laminin isoforms and is a component of the hemidesmosome. Increased expression levels of this integrin correlate with the aggressive phenotype of many epithelial tumors compared with surrounding normal tissue. Furthermore, the long cytoplasmic tail of the 4 integrin subunit has been implicated in several signal transduction pathways that are involved not only in invasion, but also in proliferation and apoptosis. Here we report that the exogenous expression of 4 integrin in 32D/v-abl-transformed cells reduces tumor aggressiveness in vivo and strongly inhibits cell proliferation in vitro by inducing monocytic differentiation. These effects are accompanied by growth arrest and p73 protein accumulation. The hypothesis that the inhibition of v-Abl oncogenic capacity could allow the activation of the endogenous c-Abl was tested in RKO cells. The results clearly demonstrated a strong increase of c-Abl phosphorylation that is accompanied by its association with p73 protein. Overall, the reported findings indicate that 64 integrin promotes growth arrest and differentiation by modulating Abl kinases and p73 protein pathway(s). © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Marques-Garcia, N. Ferrandiz, R. Fernandez-Alonso, L. Gonzalez-Cano, M. Herreros-Villanueva, M. Rosa-Garrido, B. Fernandez-Garcia, J. P. Vaque, M. M. Marques, M. E. Alonso, et al. p73 Plays a Role in Erythroid Differentiation through GATA1 Induction J. Biol. Chem., August 7, 2009; 284(32): 21139 - 21156. [Abstract] [Full Text] [PDF] A. F. List, J. Vardiman, J.-P. J. Issa, and T. M. DeWitte Myelodysplastic Syndromes Hematology, January 1, 2004; 2004(1): 297 - 317. [Abstract] [Full Text] [PDF] G. Fontemaggi, I. Kela, N. Amariglio, G. Rechavi, J. Krishnamurthy, S. Strano, A. Sacchi, D. Givol, and G. Blandino Identification of Direct p73 Target Genes Combining DNA Microarray and Chromatin Immunoprecipitation Analyses J. Biol. Chem., November 1, 2002; 277(45): 43359 - 43368. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020