Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오구택 | * |
dc.date.accessioned | 2016-08-28T10:08:23Z | - |
dc.date.available | 2016-08-28T10:08:23Z | - |
dc.date.issued | 2012 | * |
dc.identifier.issn | 0898-6568 | * |
dc.identifier.other | OAK-8947 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222787 | - |
dc.description.abstract | Macrophage inhibitory cytokine-1 (MIC-1) is highly associated with malignant human cancers and has been suggested to be involved in tumor angiogenesis. In the present study, we examined the effect of MIC-1 on endothelial cell proliferation to confirm the angiogenesis-promoting role of MIC-1. MIC-1 treatment accelerated progression of the G1 stage in the cell cycle of human umbilical vein endothelial cells (HUVECs), leading to an increased cell proliferation rate. MIC-1 augmented the levels of cyclins D1 and E without altering the levels of cyclin-dependent kinase (CDK) inhibitors, thereby increasing protein kinase activity of CDKs and subsequent phosphorylation of the Rb protein followed by nuclear translocation of E2F. MIC-1-induced expression of cyclins D1 and E was mediated by AP-1 and E2F-1 transcription factors, and among the AP-1 members, c-Jun and JunD appeared to participate in MIC-1-dependent transcription of the cyclin D1 gene. Additionally, the PI3K/Akt, JNK, and ERK pathways were found to mediate MIC-1-induced cyclin D1 expression in HUVECs. Importantly, lung endothelial cells isolated from MIC-1 transgenic mouse displayed a higher proliferation rate and cyclin D1 and E levels relative to their wild-type counterparts. These results suggest that MIC-1 secreted from cancer cells stimulates endothelial cell proliferation by enhancing AP-1- and E2F-dependent expression of G1 cyclins via PI3K/Akt, JNK, and ERK signaling pathways, potentially leading to enhanced tumor angiogenesis. © 2012 Elsevier Inc. | * |
dc.language | English | * |
dc.title | Macrophage inhibitory cytokine-1 stimulates proliferation of human umbilical vein endothelial cells by up-regulating cyclins D1 and E through the PI3K/Akt-, ERK-, and JNK-dependent AP-1 and E2F activation signaling pathways | * |
dc.type | Article | * |
dc.relation.issue | 8 | * |
dc.relation.volume | 24 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1485 | * |
dc.relation.lastpage | 1495 | * |
dc.relation.journaltitle | Cellular Signalling | * |
dc.identifier.doi | 10.1016/j.cellsig.2012.03.014 | * |
dc.identifier.wosid | WOS:000305712800002 | * |
dc.identifier.scopusid | 2-s2.0-84861541413 | * |
dc.author.google | Jin Y.-J. | * |
dc.author.google | Lee J.-H. | * |
dc.author.google | Kim Y.-M. | * |
dc.author.google | Oh G.T. | * |
dc.author.google | Lee H. | * |
dc.contributor.scopusid | 오구택(7007056663) | * |
dc.date.modifydate | 20240123094756 | * |