Vascular RhoJ Is an Effective and Selective Target for Tumor Angiogenesis and Vascular Disruption

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dc.contributor.authorKim, Chanko
dc.contributor.authorYang, Hanseulko
dc.contributor.authorFukushima, Yokoko
dc.contributor.authorSaw, Phei Erko
dc.contributor.authorLee, Junyeopko
dc.contributor.authorPark, Jin-Sungko
dc.contributor.authorPark, Intaeko
dc.contributor.authorJung, Jinmyungko
dc.contributor.authorKataoka, Hiroshiko
dc.contributor.authorLee, Doheonko
dc.contributor.authorHeo, Won Doko
dc.contributor.authorKim, Injuneko
dc.contributor.authorJon, Sangyongko
dc.contributor.authorAdams, Ralf H.ko
dc.contributor.authorNishikawa, Shin-Ichiko
dc.contributor.authorUemura, Akiyoshiko
dc.contributor.authorKoh, Gou Youngko
dc.date.accessioned2014-09-02-
dc.date.available2014-09-02-
dc.date.created2014-01-24-
dc.date.created2014-01-24-
dc.date.created2014-01-24-
dc.date.created2014-01-24-
dc.date.issued2014-01-
dc.identifier.citationCANCER CELL, v.25, no.1, pp.102 - 117-
dc.identifier.issn1535-6108-
dc.identifier.urihttp://hdl.handle.net/10203/189715-
dc.description.abstractCurrent antiangiogenic therapy is limited by its cytostatic nature and systemic side effects. To address these limitations, we have unveiled the role of RhoJ, an endothelial-enriched Rho GTPase, during tumor progression. RhoJ blockade provides a double assault on tumor vessels by both inhibiting tumor angiogenesis and disrupting the preformed tumor vessels through the activation of the RhoA-ROCK (Rho kinase) signaling pathway in tumor endothelial cells, consequently resulting in a functional failure Of tumor vasculatures. Moreover, enhanced anticancer effects were observed when RhoJ blockade was employed in concert with a cytotoxic chemotherapeutic agent, angiogenesis-inhibiting agent, or vascular-disrupting agent. These results identify RhoJ blockade as a selective and effective therapeutic strategy for targeting tumor vasculature with minimal side effects.-
dc.languageEnglish-
dc.publisherCELL PRESS-
dc.titleVascular RhoJ Is an Effective and Selective Target for Tumor Angiogenesis and Vascular Disruption-
dc.typeArticle-
dc.identifier.wosid000330819900013-
dc.identifier.scopusid2-s2.0-84892414410-
dc.type.rimsART-
dc.citation.volume25-
dc.citation.issue1-
dc.citation.beginningpage102-
dc.citation.endingpage117-
dc.citation.publicationnameCANCER CELL-
dc.identifier.doi10.1016/j.ccr.2013.12.010-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.contributor.localauthorYang, Hanseul-
dc.contributor.localauthorLee, Doheon-
dc.contributor.localauthorHeo, Won Do-
dc.contributor.localauthorKim, Injune-
dc.contributor.localauthorJon, Sangyong-
dc.contributor.localauthorKoh, Gou Young-
dc.contributor.nonIdAuthorKim, Chan-
dc.contributor.nonIdAuthorFukushima, Yoko-
dc.contributor.nonIdAuthorSaw, Phei Er-
dc.contributor.nonIdAuthorPark, Intae-
dc.contributor.nonIdAuthorJung, Jinmyung-
dc.contributor.nonIdAuthorKataoka, Hiroshi-
dc.contributor.nonIdAuthorAdams, Ralf H.-
dc.contributor.nonIdAuthorNishikawa, Shin-Ichi-
dc.contributor.nonIdAuthorUemura, Akiyoshi-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusCLINICAL-APPLICATIONS-
dc.subject.keywordPlusDRUG-RESISTANCE-
dc.subject.keywordPlusBLOOD-VESSELS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusTHERAPY-
dc.subject.keywordPlusAGENTS-
dc.subject.keywordPlusGTPASE-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusMICROENVIRONMENT-
dc.subject.keywordPlusCOMBINATION-
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