https://scholars.lib.ntu.edu.tw/handle/123456789/458257
DC Field | Value | Language |
---|---|---|
dc.contributor.author | LING-HUNG WEI | en_US |
dc.contributor.author | Kuo M.-L | en_US |
dc.contributor.author | CHI-AN CHEN | en_US |
dc.contributor.author | Chou C.-H | en_US |
dc.contributor.author | Lai K.-B | en_US |
dc.contributor.author | CHIEN-NAN LEE | en_US |
dc.contributor.author | CHANG-YAO HSIEH | en_US |
dc.creator | Hsieh C.-Y.;Lee C.-N;Lai K.-B;Chou C.-H;Chen C.-A;Kuo M.-L;LING-HUNG WEI | - |
dc.date.accessioned | 2020-02-12T05:48:34Z | - |
dc.date.available | 2020-02-12T05:48:34Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/458257 | - |
dc.description.abstract | Interleukin-6 (IL-6) has received particular attention in the pathogenesis of cervical cancer, although the underlying mechanism remains elusive. This study revealed that IL-6 promotes in vivo tumor growth of human cervical cancer C33A cells, but does not substantially alter their in vitro growth kinetics. The in vivo angiogenic assays showed that IL-6 increases angiogenic activity in human cervical cancer cells, an effect that is specifically associated with upregulation of vascular endothelial growth factor (VEGF). Also, using anti-VEGF antibody to block VEGF function significantly inhibited IL-6-mediated angiogenesis and tumor growth in nude mice, strongly supporting the critical role of VEGF in the IL-6-mediated cervical tumorigenesis. Accordingly, the signaling pathway downstream of IL-6/ IL-6R responsible for the regulation of VEGF was investigated. Notably, pharmacological inhibition of PI3-K or MAPK failed to inhibit IL-6-mediated transcriptional upregulation of VEGF. Meanwhile, blocking STAT3 pathway with dominant-negative mutant STAT3D effectively abolished IL-6-induced VEGF mRNA. In transient transfections, a luciferase reporter construct containing the full-length 1.5-kb VEGF promoter or a 1.2-kb fragment lacking the known hypoxic-response element also exhibited the same degree of response to IL-6. Additionally, transient transfection of STAT3D downregulated the 1.2-kb VEGF promoter luciferase reporter stimulated by IL-6. Based on the above phenomenon combined with the concomitant increased tumor expression of IL-6 and VEGF in cervical cancer tissues, we conclude that IL-6 may promote cervical tumorigenesis by activating VEGF-mediated angiogenesis via a STAT3 pathway. | - |
dc.relation.ispartof | Oncogene | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | interleukin 6; interleukin 6 receptor; luciferase; mitogen activated protein kinase; phosphatidylinositol 3 kinase; STAT3 protein; vasculotropin; angiogenesis; animal experiment; animal model; article; cancer growth; controlled study; down regulation; genetic transcription; human; human cell; hypoxia; mouse; nonhuman; nude mouse; priority journal; protein expression; reporter gene; signal transduction; upregulation; uterine cervix cancer; Animals; Antibodies, Monoclonal; Carcinogenicity Tests; Cell Division; Cervix Uteri; Chick Embryo; Culture Media, Conditioned; DNA-Binding Proteins; Endothelial Growth Factors; Enzyme Inhibitors; Female; Humans; Intercellular Signaling Peptides and Proteins; Interleukin-6; Lymphokines; Mice; Mice, Nude; Neovascularization, Pathologic; Reference Values; Signal Transduction; STAT3 Transcription Factor; Trans-Activators; Tumor Cells, Cultured; Up-Regulation; Uterine Cervical Neoplasms; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors; Animalia; Mus musculus | - |
dc.title | Interleukin-6 promotes cervical tumor growth by VEGF-dependent angiogenesis via a STAT3 pathway | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1038/sj.onc.1206226 | - |
dc.identifier.pmid | 12629515 | - |
dc.identifier.scopus | 2-s2.0-0037435011 | - |
dc.relation.pages | 1517-1527 | - |
dc.relation.journalvolume | 22 | - |
dc.relation.journalissue | 10 | - |
item.openairetype | journal article | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Obstetrics&Gynecology-NTUHHC | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.orcid | 0000-0001-8789-0859 | - |
crisitem.author.orcid | 0000-0001-6670-7939 | - |
crisitem.author.orcid | 0000-0002-1725-0407 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | NTU Hsin-Chu Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
Appears in Collections: | 醫學系 |
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