Show simple item record

dc.contributor.authorMorena, Annarita
dc.contributor.authorRiccioni, Sabrina
dc.contributor.authorMarchetti, Alessandra
dc.contributor.authorPolcini, Alessandro Tartaglia
dc.contributor.authorMercurio, Arthur M.
dc.contributor.authorBlandino, Giovanni
dc.contributor.authorSacchi, Ada
dc.contributor.authorFalcioni, Rita
dc.date2022-08-11T08:08:01.000
dc.date.accessioned2022-08-23T15:39:45Z
dc.date.available2022-08-23T15:39:45Z
dc.date.issued2002-06-19
dc.date.submitted2010-11-07
dc.identifier.citation<p>Blood. 2002 Jul 1;100(1):96-106.</p>
dc.identifier.issn0006-4971 (Linking)
dc.identifier.doi10.1182/blood.v100.1.96
dc.identifier.pmid12070014
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26245
dc.description.abstractThe alpha 6 beta 4 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 beta 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 beta 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 alpha 6 beta 4 integrin promotes growth arrest and differentiation by modulating Abl kinases and p73 protein pathway(s).
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12070014&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1182/blood.v100.1.96
dc.subjectAnimals
dc.subjectAntigens, Surface
dc.subjectCell Differentiation
dc.subjectCell Division
dc.subjectCell Line, Transformed
dc.subjectDNA-Binding Proteins
dc.subjectGenes, Tumor Suppressor
dc.subjectIntegrin alpha6beta4
dc.subjectIntegrins
dc.subjectMice
dc.subjectMitogen-Activated Protein Kinases
dc.subjectMonocytes
dc.subjectNeoplasm Proteins
dc.subjectNuclear Proteins
dc.subjectOncogene Proteins v-abl
dc.subjectPhosphorylation
dc.subjectProtein Subunits
dc.subjectSignal Transduction
dc.subjectTumor Suppressor Proteins
dc.subjectintegrins
dc.subjectmonocytes
dc.subjecttumor suppressor protein p73
dc.subjectcytoplasm
dc.subjectneoplasms
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectCancer Biology
dc.subjectCells
dc.subjectNeoplasms
dc.titleExpression of the beta 4 integrin subunit induces monocytic differentiation of 32D/v-Abl cells
dc.typeArticle
dc.source.journaltitleBlood
dc.source.volume100
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/159
dc.identifier.contextkey1633384
html.description.abstract<p>The alpha 6 beta 4 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 beta 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 beta 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 alpha 6 beta 4 integrin promotes growth arrest and differentiation by modulating Abl kinases and p73 protein pathway(s).</p>
dc.identifier.submissionpathcancerbiology_pp/159
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages96-106


This item appears in the following Collection(s)

Show simple item record