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dc.contributor.authorChung, Jun
dc.contributor.authorYoon, Sang-oh
dc.contributor.authorLipscomb, Elizabeth A.
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:39:49Z
dc.date.available2022-08-23T15:39:49Z
dc.date.issued2004-05-27
dc.date.submitted2010-11-07
dc.identifier.citationJ Biol Chem. 2004 Jul 30;279(31):32287-93. Epub 2004 May 25. <a href="http://dx.doi.org/10.1074/jbc.M403809200">Link to article on publisher's site</a>
dc.identifier.issn0021-9258 (Linking)
dc.identifier.doi10.1074/jbc.M403809200
dc.identifier.pmid15161909
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26261
dc.description.abstractIt has been proposed that a constitutive, physical association of the Met receptor and the alpha(6)beta(4) integrin exists on the surface of invasive carcinoma cells and that hepatocyte growth factor (HGF)-mediated invasion is dependent on alpha(6)beta(4) (Trusolino, L., Bertotti, A., and Comoglio, P. M. (2001) Cell 107, 643-654). The potential significance of these results prompted us to re-examine this hypothesis. Using three different carcinoma cell lines that express both Met and alpha(6)beta(4), we were unable to detect the constitutive association of these receptors by co-immunoprecipitation. Moreover, carcinoma cells that lacked expression of alpha(6)beta(4) exhibited Met-dependent invasion toward HGF, and increasing Met expression by viral infection of these cells enhanced invasion without inducing alpha(6)beta(4) expression. Although expression of alpha(6)beta(4) in such cells enhanced their invasion to HGF, it also enhanced their ability to invade toward other chemoattractants such as lysophosphatidic acid, and this latter invasion was not inhibited by a function-blocking Met antibody. Finally, depletion of beta(4) by RNA interference in invasive carcinoma cells that express both receptors reduced the ability of these cells to invade toward HGF by approximately 25%, but it did not abrogate their invasion. These data argue that the invasive function of Met can be independent of alpha(6)beta(4) and that alpha(6)beta(4) has a generic influence on the invasion of carcinoma cells that is not specific to Met.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15161909&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1074/jbc.M403809200
dc.subject3T3 Cells
dc.subjectAnimals
dc.subjectCarcinoma
dc.subjectCell Line, Tumor
dc.subjectCulture Media, Conditioned
dc.subjectHepatocyte Growth Factor
dc.subjectHumans
dc.subjectImmunoblotting
dc.subjectIntegrin alpha6beta4
dc.subjectIntegrin beta4
dc.subjectLysophospholipids
dc.subjectMice
dc.subjectNeoplasm Invasiveness
dc.subjectPrecipitin Tests
dc.subjectProteins
dc.subject*Proto-Oncogene Proteins
dc.subjectRNA Interference
dc.subjectRNA, Small Interfering
dc.subject*Receptors, Growth Factor
dc.subjectRetroviridae
dc.subjectTime Factors
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleThe Met receptor and alpha 6 beta 4 integrin can function independently to promote carcinoma invasion
dc.typeArticle
dc.source.journaltitleThe Journal of biological chemistry
dc.source.volume279
dc.source.issue31
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/175
dc.identifier.contextkey1633401
html.description.abstract<p>It has been proposed that a constitutive, physical association of the Met receptor and the alpha(6)beta(4) integrin exists on the surface of invasive carcinoma cells and that hepatocyte growth factor (HGF)-mediated invasion is dependent on alpha(6)beta(4) (Trusolino, L., Bertotti, A., and Comoglio, P. M. (2001) Cell 107, 643-654). The potential significance of these results prompted us to re-examine this hypothesis. Using three different carcinoma cell lines that express both Met and alpha(6)beta(4), we were unable to detect the constitutive association of these receptors by co-immunoprecipitation. Moreover, carcinoma cells that lacked expression of alpha(6)beta(4) exhibited Met-dependent invasion toward HGF, and increasing Met expression by viral infection of these cells enhanced invasion without inducing alpha(6)beta(4) expression. Although expression of alpha(6)beta(4) in such cells enhanced their invasion to HGF, it also enhanced their ability to invade toward other chemoattractants such as lysophosphatidic acid, and this latter invasion was not inhibited by a function-blocking Met antibody. Finally, depletion of beta(4) by RNA interference in invasive carcinoma cells that express both receptors reduced the ability of these cells to invade toward HGF by approximately 25%, but it did not abrogate their invasion. These data argue that the invasive function of Met can be independent of alpha(6)beta(4) and that alpha(6)beta(4) has a generic influence on the invasion of carcinoma cells that is not specific to Met.</p>
dc.identifier.submissionpathcancerbiology_pp/175
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages32287-93


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