Hypoxia Induces Paclitaxel-Resistance through ROS Production
DC Field | Value | Language |
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dc.contributor.author | Oh, Jin-Mi | - |
dc.contributor.author | Ryu, Yun-Kyoung | - |
dc.contributor.author | Lim, Jong-Seok | - |
dc.contributor.author | Moon, Eun-Yi | - |
dc.date.available | 2021-02-22T13:48:10Z | - |
dc.date.issued | 2010-04-30 | - |
dc.identifier.issn | 1976-9148 | - |
dc.identifier.issn | 2005-4483 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13221 | - |
dc.description.abstract | Oxygen supply into inside solid tumor is often diminished, which is called hypoxia. Many gene transcriptions were activated by hypoxia-inducible factor (HIF)-1 alpha. Here, we investigated the effect of hypoxia on paclitaxel-resistance induction in HeLa cervical tumor cells. When HeLa cells were incubated under hypoxia condition, HIF-1 alpha level was increased. In contrast, paclitaxel-mediated tumor cell death was reduced by the incubation under hypoxia condition. Paclitaxel-mediated tumor cell death was also inhibited by treatment with DMOG, chemical HIF-1 alpha stabilizer, in a dose-dependent manner. A significant increase in intracellular ROS level was detected by the incubation under hypoxia condition. A basal level of cell density was increased in response to 10 nM H2O2. HIF-1 alpha level was increased by treatment with various concentration of H2O2. The increased level of HIF-1 alpha by hypoxia was reduced by the treatment with N-acetylcysteine (NAC), a well-known ROS scavenger. Paclitaxel-mediated tumor cell death was increased by treatment with NAC. Taken together, these findings demonstrate that hypoxia could play a role in paclitaxel-resistance induction through ROS-mediated HIF-1 alpha stabilization. These results suggest that hypoxia-induced ROS could, in part, control tumor cell death through an increase in HIF-1 alpha level. | - |
dc.format.extent | 7 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KOREAN SOC APPLIED PHARMACOLOGY | - |
dc.title | Hypoxia Induces Paclitaxel-Resistance through ROS Production | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.doi | 10.4062/biomolther.2010.18.2.145 | - |
dc.identifier.scopusid | 2-s2.0-77953115635 | - |
dc.identifier.wosid | 000277582000003 | - |
dc.identifier.bibliographicCitation | BIOMOLECULES & THERAPEUTICS, v.18, no.2, pp 145 - 151 | - |
dc.citation.title | BIOMOLECULES & THERAPEUTICS | - |
dc.citation.volume | 18 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 145 | - |
dc.citation.endPage | 151 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART001441725 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.subject.keywordPlus | INDUCIBLE FACTOR 1-ALPHA | - |
dc.subject.keywordPlus | MITOCHONDRIAL OXYGEN-CONSUMPTION | - |
dc.subject.keywordPlus | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject.keywordPlus | OVARIAN-CANCER CELLS | - |
dc.subject.keywordPlus | FACTOR-KAPPA-B | - |
dc.subject.keywordPlus | THYMOSIN-BETA-4 TB4 | - |
dc.subject.keywordPlus | HIF-1-ALPHA PROTEIN | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordAuthor | HeLa cell | - |
dc.subject.keywordAuthor | Hypoxia | - |
dc.subject.keywordAuthor | HIF-1 alpha | - |
dc.subject.keywordAuthor | ROS | - |
dc.subject.keywordAuthor | Paclitaxel | - |
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