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dc.contributor.authorZhang, Aoen
dc.contributor.authorHitomi, Masahiroen
dc.contributor.authorBar-Shain, Noahen
dc.contributor.authorDalimov, Zafardjanen
dc.contributor.authorEllis, Leighen
dc.contributor.authorVelpula, Kiran K.en
dc.contributor.authorFraizer, Gail C.en
dc.contributor.authorGourdie, Robert G.en
dc.contributor.authorLathia, Justin D.en
dc.coverage.spatialUnited Statesen
dc.date.accessioned2017-02-09T20:21:16Zen
dc.date.available2017-02-09T20:21:16Zen
dc.date.issued2015-05-10en
dc.identifier.urihttp://hdl.handle.net/10919/74987en
dc.description.abstractImpaired expression of connexins, the gap junction subunits that facilitate direct cell-cell communication, have been implicated in prostate cancer growth. To elucidate the crucial role of connexins in prostate cancer progression, we performed a systematic quantitative RT-PCR screening of connexin expression in four representative prostate cancer cell lines across the spectrum of malignancy. Transcripts of several connexin subunits were detected in all four cell lines, and connexin 43 (Cx43) showed marked elevation at both RNA and protein levels in cells with increased metastatic potential. Analysis of gap-junction-mediated intercellular communication revealed homocellular coupling in PC-3 cells, which had the highest C x 43 expression, with minimal coupling in LNCaP cells where C x 43 expression was very low. Treatment with the gap junction inhibitor carbenoxolone or connexin mimetic peptide ACT-1 did not impair cell growth, suggesting that growth is independent of functional gap junctions. PC-3 cells with C x 43 expression reduced by shRNA showed decreased migration in monolayer wound healing assay, as well as decreased transwell invasion capacities when compared to control cells expressing non-targeting shRNA. These results, together with the correlation between C x 43 expression levels and the metastatic capacity of the cell lines, suggest a role of C x 43 in prostate cancer invasion and metastasis.en
dc.format.extent11640 - 11651 page(s)en
dc.languageengen
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/25960544en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectCx43en
dc.subjectgap junction independent functionen
dc.subjectinvasionen
dc.subjectprostate canceren
dc.subjectAnimalsen
dc.subjectCell Line, Tumoren
dc.subjectCell Movementen
dc.subjectCell Proliferationen
dc.subjectConnexin 43en
dc.subjectGap Junctionsen
dc.subjectGene Expression Regulation, Neoplasticen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectNeoplasm Invasivenessen
dc.subjectNeoplasm Metastasisen
dc.subjectProstatic Neoplasmsen
dc.subjectRNA Interferenceen
dc.subjectRNA, Messengeren
dc.subjectReal-Time Polymerase Chain Reactionen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectSignal Transductionen
dc.subjectTime Factorsen
dc.subjectTransfectionen
dc.titleConnexin 43 expression is associated with increased malignancy in prostate cancer cell lines and functions to promote migration.en
dc.typeArticle - Refereeden
dc.description.versionPublished (Publication status)en
dc.contributor.departmentBiomedical Engineering and Mechanicsen
dc.contributor.departmentFralin Biomedical Research Instituteen
dc.title.serialOncotargeten
dc.identifier.doihttps://doi.org/10.18632/oncotarget.3449en
dc.type.otherResearch Support, N.I.H., Extramuralen
dc.type.otherResearch Support, Non-U.S. Gov'ten
dc.identifier.volume6en
dc.identifier.issue13en
dc.identifier.eissn1949-2553en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/University Research Institutesen
pubs.organisational-group/Virginia Tech/University Research Institutes/Virginia Tech Carilion Research Instituteen


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