Activated STAT3 Regulates Hypoxia-Induced Angiogenesis and Cell Migration in Human Glioblastoma
DC Field | Value | Language |
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dc.contributor.author | Kang, Shin-Hyuk | - |
dc.contributor.author | Yu, Mi Ok | - |
dc.contributor.author | Park, Kyung-Jae | - |
dc.contributor.author | Chi, Sung-Gil | - |
dc.contributor.author | Park, Dong-Hyuk | - |
dc.contributor.author | Chung, Yong-Gu | - |
dc.date.accessioned | 2021-09-07T23:04:34Z | - |
dc.date.available | 2021-09-07T23:04:34Z | - |
dc.date.created | 2021-06-14 | - |
dc.date.issued | 2010-11 | - |
dc.identifier.issn | 0148-396X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/115371 | - |
dc.description.abstract | BACKGROUND: Glioblastoma is the most common primary brain tumor, with typical histopathologic findings, pseudopalisading necrosis, and microvascular proliferation, all of which are associated with a poor prognosis. Hypoxia is known to affect these morphological features, but the underlying molecular mechanism has been poorly understood. OBJECTIVE: To determine the role of signal transducer and activator of transcription 3 (STAT3) in the malignant progression of glioblastoma under hypoxic conditions. METHODS: We studied STAT3 activation by hypoxic stress and its effect on hypoxia-induced angiogenesis and cell migration using U87, A172, T98, and U373 human glioblastoma cell lines. RESULTS: All four glioblastoma cells analyzed expressed detectable levels of STAT3 phosphorylation. Hypoxic stress markedly increased phosphorylated STAT3 level in a time-dependent fashion, and activated STAT3 was translocated into the nucleus. Hypoxic conditions led to a 30-50% increase in angiogenesis and cell migration, but these effects were significantly attenuated by small interfering ribonucleic acid-mediated knockdown of STAT3. Furthermore, STAT3 activation was associated with an elevated expression of hypoxic inducible factor-1, vascular endothelial growth factor, matrix metalloproteinase 2, and TWIST messenger ribonucleic acid and protein, which may play a critical role in hypoxia-induced angiogenesis and migration. CONCLUSION: STAT3 plays an important role in glioblastoma angiogenesis and migration triggered by hypoxia. Therefore, STAT3 might be a target for control of pseudopalisading necrosis and angiogenesis in glioblastoma. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | OXFORD UNIV PRESS INC | - |
dc.subject | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject | INDUCIBLE FACTOR-1 | - |
dc.subject | SIGNAL TRANSDUCER | - |
dc.subject | VEGF EXPRESSION | - |
dc.subject | FACTOR GENE | - |
dc.subject | BRAIN-TUMORS | - |
dc.subject | GLIOMA-CELLS | - |
dc.subject | TRANSCRIPTION-3 | - |
dc.subject | APOPTOSIS | - |
dc.subject | INVASION | - |
dc.title | Activated STAT3 Regulates Hypoxia-Induced Angiogenesis and Cell Migration in Human Glioblastoma | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kang, Shin-Hyuk | - |
dc.contributor.affiliatedAuthor | Park, Kyung-Jae | - |
dc.contributor.affiliatedAuthor | Chi, Sung-Gil | - |
dc.contributor.affiliatedAuthor | Park, Dong-Hyuk | - |
dc.identifier.doi | 10.1227/NEU.0b013e3181f1c0cd | - |
dc.identifier.scopusid | 2-s2.0-77958512917 | - |
dc.identifier.wosid | 000283479500048 | - |
dc.identifier.bibliographicCitation | NEUROSURGERY, v.67, no.5, pp.1386 - 1395 | - |
dc.relation.isPartOf | NEUROSURGERY | - |
dc.citation.title | NEUROSURGERY | - |
dc.citation.volume | 67 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 1386 | - |
dc.citation.endPage | 1395 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalResearchArea | Surgery | - |
dc.relation.journalWebOfScienceCategory | Clinical Neurology | - |
dc.relation.journalWebOfScienceCategory | Surgery | - |
dc.subject.keywordPlus | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject.keywordPlus | INDUCIBLE FACTOR-1 | - |
dc.subject.keywordPlus | SIGNAL TRANSDUCER | - |
dc.subject.keywordPlus | VEGF EXPRESSION | - |
dc.subject.keywordPlus | FACTOR GENE | - |
dc.subject.keywordPlus | BRAIN-TUMORS | - |
dc.subject.keywordPlus | GLIOMA-CELLS | - |
dc.subject.keywordPlus | TRANSCRIPTION-3 | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | INVASION | - |
dc.subject.keywordAuthor | Angiogenesis | - |
dc.subject.keywordAuthor | Glioblastoma | - |
dc.subject.keywordAuthor | Hypoxia | - |
dc.subject.keywordAuthor | Migration | - |
dc.subject.keywordAuthor | Signal transducer and activator of transcription 3 | - |
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