Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 권영주 | * |
dc.date.accessioned | 2016-08-29T12:08:39Z | - |
dc.date.available | 2016-08-29T12:08:39Z | - |
dc.date.issued | 2015 | * |
dc.identifier.issn | 1949-2553 | * |
dc.identifier.other | OAK-15891 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/230871 | - |
dc.description.abstract | The suppressor of MEK null (sMEK1) protein possesses pro-apoptotic activities. In the current study, we reveal that sMEK1 functions as a novel anti-angiogenic factor by suppressing vascular endothelial growth factor (VEGF)-induced cell proliferation, migration, and capillary-like tubular structure in vitro. In addition, sMEK1 inhibited the phosphorylation of the signaling components up- and downstream of Akt, including phospholipase Cγ1 (PLC-γ1), 3-phosphoinositide-dependent protein kinase 1 (PDK1), endothelial nitric oxide synthetase (eNOS), and hypoxia-inducible factor 1 (HIF-1α) during ovarian tumor progression via binding with vascular endothelial growth factor receptor 2 (VEGFR-2). Furthermore, sMEK1 decreased tumor vascularity and inhibited tumor growth in a xenograft human ovarian tumor model. These results supply convincing evidence that sMEK1 controls endothelial cell function and subsequent angiogenesis by suppressing VEGFR-2-mediated PI3K/Akt/eNOS signaling pathway. Taken together, our results clearly suggest that sMEK1 might be a novel antiangiogenic and anti-tumor agent for use in ovarian tumor. | * |
dc.language | English | * |
dc.publisher | Impact Journals LLC | * |
dc.subject | Anti-angiogenic activity | * |
dc.subject | Hypoxic condition | * |
dc.subject | Ovarian tumor | * |
dc.subject | sMEK1 tumor suppressor | * |
dc.subject | Xenograft model | * |
dc.title | sMEK1 inhibits endothelial cell proliferation by attenuating VEGFR-2-dependent-Akt/eNOS/HIF-1α signaling pathways | * |
dc.type | Article | * |
dc.relation.issue | 31 | * |
dc.relation.volume | 6 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 31830 | * |
dc.relation.lastpage | 31843 | * |
dc.relation.journaltitle | Oncotarget | * |
dc.identifier.doi | 10.18632/oncotarget.5570 | * |
dc.identifier.scopusid | 2-s2.0-84945535957 | * |
dc.author.google | Kim | * |
dc.author.google | B.-R. | * |
dc.author.google | Seo | * |
dc.author.google | S.H. | * |
dc.author.google | Park | * |
dc.author.google | M.S. | * |
dc.author.google | Lee | * |
dc.author.google | S.-H. | * |
dc.author.google | Kwon | * |
dc.author.google | Y. | * |
dc.author.google | Rho | * |
dc.author.google | S.B. | * |
dc.contributor.scopusid | 권영주(12446435600) | * |
dc.date.modifydate | 20240422124907 | * |