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Angiogenesis and vasculogenic mimicry as therapeutic targets in ovarian cancer

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dc.contributor.authorLim, Dansaem-
dc.contributor.authorDo, Yeojin-
dc.contributor.authorKwon, Byung Su-
dc.contributor.authorChang, Woochul-
dc.contributor.authorLee, Myeong-Sok-
dc.contributor.authorKim, Jongmin-
dc.contributor.authorCho, Jin Gu-
dc.date.available2021-02-22T05:24:32Z-
dc.date.issued2020-06-
dc.identifier.issn1976-6696-
dc.identifier.issn1976-670X-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/1472-
dc.description.abstractTumor angiogenesis is an essential process for growth and metastasis of cancer cells as it supplies tumors with oxygen and nutrients. During tumor angiogenesis, many pro-angiogenic factors are secreted by tumor cells to induce their own vascularization via activation of pre-existing host endothelium. However, accumulating evidence suggests that vasculogenic mimicry (VM) is a key alternative mechanism for tumor vascularization when tumors are faced with insufficient supply of oxygen and nutrients. VM is a tumor vascularization mechanism in which tumors create a blood supply system, in contrast to tumor angiogenesis mechanisms that depend on pre-existing host endothelium. VM is closely associated with tumor progression and poor prognosis in many cancels. Therefore, inhibition of VM may be a promising therapeutic strategy and may overcome the limitations of anti-angiogenesis therapy for cancer patients. In this review, we provide an overview of the current anti-angiogenic therapies for ovarian cancer and the current state of knowledge regarding the links between microRNAs and the VM process, with a focus on the mechanism that regulates associated signaling pathways in ovarian cancer. Moreover, we discuss the potential for VM as a therapeutic strategy against ovarian cancer.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.titleAngiogenesis and vasculogenic mimicry as therapeutic targets in ovarian cancer-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.5483/BMBRep.2020.53.6.060-
dc.identifier.scopusid2-s2.0-85087111009-
dc.identifier.wosid000545933200001-
dc.identifier.bibliographicCitationBMB REPORTS, v.53, no.6, pp 291 - 298-
dc.citation.titleBMB REPORTS-
dc.citation.volume53-
dc.citation.number6-
dc.citation.startPage291-
dc.citation.endPage298-
dc.type.docTypeReview-
dc.identifier.kciidART002598592-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.subject.keywordPlusENDOTHELIAL-GROWTH-FACTOR-
dc.subject.keywordPlusEPITHELIAL-MESENCHYMAL TRANSITION-
dc.subject.keywordPlusHUMAN-MELANOMA CELLS-
dc.subject.keywordPlusDOUBLE-BLIND-
dc.subject.keywordPlusFUNCTIONAL-SIGNIFICANCE-
dc.subject.keywordPlusCLINICAL-SIGNIFICANCE-
dc.subject.keywordPlusMOLECULAR-MECHANISMS-
dc.subject.keywordPlusCHANNEL FORMATION-
dc.subject.keywordPlusTUMOR-GROWTH-
dc.subject.keywordPlusVE-CADHERIN-
dc.subject.keywordAuthorAngiogenesis-
dc.subject.keywordAuthorOvarian cancer-
dc.subject.keywordAuthorTherapeutic target-
dc.subject.keywordAuthorTumor vascularization-
dc.subject.keywordAuthorVasculogenic mimicry-
dc.identifier.urlhttp://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2020.53.6.060-
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