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dc.contributor.authorGoel, Hira Lal
dc.contributor.authorUnderwood, Jean M.
dc.contributor.authorNickerson, Jeffrey A.
dc.contributor.authorHsieh, Chung-Cheng
dc.contributor.authorLanguino, Lucia R.
dc.date2022-08-11T08:09:30.000
dc.date.accessioned2022-08-23T16:33:24Z
dc.date.available2022-08-23T16:33:24Z
dc.date.issued2010-07-25
dc.date.submitted2011-02-23
dc.identifier.citationJ Cell Physiol. 2010 Jul;224(1):210-7. <a href="http://dx.doi.org/10.1002/jcp.22116">Link to article on publisher's site</a>
dc.identifier.issn0021-9541 (Linking)
dc.identifier.doi10.1002/jcp.22116
dc.identifier.pmid20333644
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38098
dc.description.abstractThe beta1 integrins play an important role in the modulation of cancer cell proliferation and tumor growth. We have previously shown that beta1 integrins associate with insulin-like growth factor type 1 receptor (IGF-IR) and regulate IGF-stimulated prostate cancer cell proliferation. In the present study, we find that downregulation of beta1 in prostate cancer cells inhibits IGF-IR and AKT activation. We also show that beta1 downregulation in two- and three-dimensional (3D) prostate cancer cell cultures significantly reduces expression of GLI1, a transcription factor known to be regulated by the IGF/AKT signaling pathway and to be a downstream effector of sonic hedgehog. Re-expression of GLI1 rescues the inhibitory effect of beta1 downregulation on prostate cancer cell proliferation in 3D cultures. We find that downregulation of beta1 significantly reduces surface expression of the associated alpha 5 integrin subunit. Our results indicate that the beta1/IGF-IR complex regulates expression of GLI1, which in turn promotes cancer cell proliferation in 3D cultures.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20333644&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/jcp.22116
dc.subjectAntigens, CD29
dc.subjectCell Culture Techniques
dc.subjectCell Line, Tumor
dc.subject*Cell Proliferation
dc.subjectHumans
dc.subjectInsulin-Like Growth Factor I
dc.subjectIntegrin alpha5
dc.subjectMale
dc.subjectPhosphorylation
dc.subjectProstatic Neoplasms
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectRNA Interference
dc.subjectReceptor, IGF Type 1
dc.subjectRecombinant Fusion Proteins
dc.subjectSignal Transduction
dc.subjectTranscription Factors
dc.subjectTransfection
dc.subjectTyrosine
dc.subjectCell Biology
dc.titleBeta1 integrins mediate cell proliferation in three-dimensional cultures by regulating expression of the sonic hedgehog effector protein, GLI1
dc.typeJournal Article
dc.source.journaltitleJournal of cellular physiology
dc.source.volume224
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/nickerson/1
dc.identifier.contextkey1809755
html.description.abstract<p>The beta1 integrins play an important role in the modulation of cancer cell proliferation and tumor growth. We have previously shown that beta1 integrins associate with insulin-like growth factor type 1 receptor (IGF-IR) and regulate IGF-stimulated prostate cancer cell proliferation. In the present study, we find that downregulation of beta1 in prostate cancer cells inhibits IGF-IR and AKT activation. We also show that beta1 downregulation in two- and three-dimensional (3D) prostate cancer cell cultures significantly reduces expression of GLI1, a transcription factor known to be regulated by the IGF/AKT signaling pathway and to be a downstream effector of sonic hedgehog. Re-expression of GLI1 rescues the inhibitory effect of beta1 downregulation on prostate cancer cell proliferation in 3D cultures. We find that downregulation of beta1 significantly reduces surface expression of the associated alpha 5 integrin subunit. Our results indicate that the beta1/IGF-IR complex regulates expression of GLI1, which in turn promotes cancer cell proliferation in 3D cultures.</p>
dc.identifier.submissionpathnickerson/1
dc.contributor.departmentDepartment of Cancer Biology and the Cancer Center
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages210-7


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