Hypoxia-induced fibroblast growth factor 11 stimulates capillary-like endothelial tube formation SCIE SCOPUS

DC Field Value Language
dc.contributor.author Yang, Jimin -
dc.contributor.author Kim, Woo Jean -
dc.contributor.author Jun, Hyoung Oh -
dc.contributor.author Lee, Eun Ju -
dc.contributor.author Lee, Kyeong Won -
dc.contributor.author Jeong, Jae-Yeon -
dc.contributor.author Lee, Sae-Won -
dc.date.accessioned 2020-04-20T03:25:16Z -
dc.date.available 2020-04-20T03:25:16Z -
dc.date.created 2020-01-28 -
dc.date.issued 2015-11 -
dc.identifier.issn 1021-335X -
dc.identifier.uri https://sciwatch.kiost.ac.kr/handle/2020.kiost/2380 -
dc.description.abstract Low oxygen or hypoxia can be observed in the central region of solid tumors. Hypoxia is a strong stimulus for new blood vessel formation or angiogenesis, which is essential for tumor growth and progression. Fibroblast growth factor 11 (FGF11) is an intracellular non-secretory FGF whose function has not yet been fully characterized. In the present study, we demonstrated that FGF11 expression is upregulated under hypoxic conditions in human umbilical vein endothelial cells (HUVECs). FGF11 overexpression stimulated capillary-like tube formation, yet did not affect cell migration. Notably, FGF11 markedly increased the levels of tight junction proteins including occludin, zonula occludens-1 (ZO-1) and claudin-5 in HUVECs. The FGF11 promoter contains hypoxia response elements (HREs), and hypoxia-inducible factor-1 (HIF-1) binds to HREs to activate hypoxia-related genes. We demonstrated that hypoxia or HIF-1 expression under normoxic conditions increased the luciferase activity driven by the FGF11 promoter. However, deletion of the HREs from the FGF11 promoter rendered reporter gene activity unresponsive to hypoxia or HIF-1. Taken together, we propose that FGF11 may be involved in the stabilization of capillary-like tube structures associated with angiogenesis and may act as a modulator of hypoxia-induced pathological processes such as tumorigenesis. -
dc.description.uri 1 -
dc.language English -
dc.publisher SPANDIDOS PUBL LTD -
dc.subject CLAUDIN 5 EXPRESSION -
dc.subject ANGIOGENESIS -
dc.subject PROTEIN -
dc.subject DIFFERENTIATION -
dc.subject MODULATION -
dc.subject MECHANISMS -
dc.subject APOPTOSIS -
dc.subject CELLS -
dc.subject VEGF -
dc.title Hypoxia-induced fibroblast growth factor 11 stimulates capillary-like endothelial tube formation -
dc.type Article -
dc.citation.endPage 2751 -
dc.citation.startPage 2745 -
dc.citation.title ONCOLOGY REPORTS -
dc.citation.volume 34 -
dc.citation.number 5 -
dc.identifier.bibliographicCitation ONCOLOGY REPORTS, v.34, no.5, pp.2745 - 2751 -
dc.identifier.doi 10.3892/or.2015.4223 -
dc.identifier.scopusid 2-s2.0-84941953339 -
dc.identifier.wosid 000362857300063 -
dc.type.docType Article -
dc.description.journalClass 1 -
dc.subject.keywordPlus CLAUDIN 5 EXPRESSION -
dc.subject.keywordPlus ANGIOGENESIS -
dc.subject.keywordPlus PROTEIN -
dc.subject.keywordPlus DIFFERENTIATION -
dc.subject.keywordPlus MODULATION -
dc.subject.keywordPlus MECHANISMS -
dc.subject.keywordPlus APOPTOSIS -
dc.subject.keywordPlus CELLS -
dc.subject.keywordPlus VEGF -
dc.subject.keywordAuthor tumor angiogenesis -
dc.subject.keywordAuthor hypoxia-inducible factor-1 -
dc.subject.keywordAuthor hypoxia response element -
dc.subject.keywordAuthor growth factor -
dc.subject.keywordAuthor transcription factor -
dc.subject.keywordAuthor fibroblast growth factor 11 -
dc.relation.journalWebOfScienceCategory Oncology -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.relation.journalResearchArea Oncology -
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Marine Resources Research Division > Marine Biotechnology Research Center > 1. Journal Articles
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