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The expression of human papillomavirus type 16 (HPV16 E7) induces cell cycle arrest and apoptosis in radiation and hypoxia resistant glioblastoma cells.
DC Field | Value | Language |
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dc.contributor.author | 문승욱 | - |
dc.contributor.author | 박경아 | - |
dc.contributor.author | 이원택 | - |
dc.contributor.author | 이종은 | - |
dc.date.accessioned | 2014-12-20T17:07:43Z | - |
dc.date.available | 2014-12-20T17:07:43Z | - |
dc.date.issued | 2011 | - |
dc.identifier.issn | 1791-2997 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/94015 | - |
dc.description.abstract | p53 is a widely known tumor-suppressor gene product that plays a key role in apoptotic cell death induced by DNA-damaging chemotherapeutic agents. Human glioma cells with functional p53 are known to be more resistant to γ-radiation. The aim of this study was to investigate whether the mutant glioblastoma cells (U87MG) transfected with human papilloma virus-type 16 E7 (HPV16 E7) genes were capable of increasing sensitivity towards irradiation and hypoxia-induced cell death. The pLXSN retroviral vector expressed HPV-16E7 genes and was infected into the p53 mutated U87MG cell line. A specific amplification band of HPV16 E7 genes was detected in E7 genes and transfected in the U87MG cell line using a reverse transcriptase polymerase chain reaction. The experimental groups included the mutant glioblastoma cell line (U87MG), empty vector (pLXSN) transfected to mutant glioblastoma cell line (U87MG-LXSN), and retrovirus carrying HPV16 E7 genes transfected to the mutant glioblastoma cell line (U87MG-E7). Hypoxic conditions were optimized using LDH assay and the subjects were exposed to hypoxia (16 and 20 h) and irradiation (9 h). Hoechst-propidium iodide (PI) staining results showed that hypoxia and irradiation increased the number of dead cells in the U87MG-E7 cells compared to U87MG and U87MG-LXSN cells. Results of the FACS analysis showed a similar pattern and recorded 80.44 and 58.94% of apoptotic cells in U87MG-E7 and U87MG cells, respectively. Cell cycle analysis by FACS revealed that, following irradiation and hypoxia, cells showed G2-M arrest. Additionally, the Western blot analysis results showed altered expression of E2F-1, Rb and p53 in the irradiation- and hypoxia-induced U87MG-E7 cells compared to U87MG and U87MG LXSN cells. In conclusion, the over-expression of HPV16 E7 genes in U87MG cell lines increasd cell apoptosis and E2F1 expression compared to the HPV non-infected U87MG cells following irradiation and hypoxia. These results indicate that tumor-specific therapies that increase sensitivity towards radiation and hypoxic conditions may be beneficial for suppression of cancers | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1247~1253 | - |
dc.relation.isPartOf | MOLECULAR MEDICINE REPORTS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Apoptosis/radiation effects* | - |
dc.subject.MESH | Cell Cycle Checkpoints/radiation effects* | - |
dc.subject.MESH | Cell Hypoxia* | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | E2F1 Transcription Factor/metabolism | - |
dc.subject.MESH | Gamma Rays | - |
dc.subject.MESH | Genetic Vectors/chemistry | - |
dc.subject.MESH | Genetic Vectors/metabolism | - |
dc.subject.MESH | Glioblastoma/pathology | - |
dc.subject.MESH | Glioblastoma/radiotherapy* | - |
dc.subject.MESH | Human papillomavirus 16/genetics* | - |
dc.subject.MESH | Human papillomavirus 16/metabolism | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Papillomavirus E7 Proteins/metabolism | - |
dc.subject.MESH | Retinoblastoma Protein/metabolism | - |
dc.subject.MESH | Retroviridae/genetics | - |
dc.subject.MESH | Transfection | - |
dc.subject.MESH | Tumor Suppressor Protein p53/genetics | - |
dc.subject.MESH | Tumor Suppressor Protein p53/metabolism | - |
dc.title | The expression of human papillomavirus type 16 (HPV16 E7) induces cell cycle arrest and apoptosis in radiation and hypoxia resistant glioblastoma cells. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Anatomy (해부학) | - |
dc.contributor.googleauthor | Sung-Ung Moon | - |
dc.contributor.googleauthor | Soo Kyoung Choi | - |
dc.contributor.googleauthor | Han Jo Kim | - |
dc.contributor.googleauthor | Kiran Kumar Bokara | - |
dc.contributor.googleauthor | Kyung Ah Park | - |
dc.contributor.googleauthor | Won Taek Lee | - |
dc.contributor.googleauthor | Jong-Eun Lee | - |
dc.identifier.doi | 10.3892/mmr.2011.561 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01368 | - |
dc.contributor.localId | A01424 | - |
dc.contributor.localId | A03007 | - |
dc.contributor.localId | A03146 | - |
dc.relation.journalcode | J02261 | - |
dc.identifier.eissn | 1791-3004 | - |
dc.identifier.pmid | 21850378 | - |
dc.contributor.alternativeName | Moon, Sung Ung | - |
dc.contributor.alternativeName | Park, Kyung Ah | - |
dc.contributor.alternativeName | Lee, Won Taek | - |
dc.contributor.alternativeName | Lee, Jong Eun | - |
dc.contributor.affiliatedAuthor | Moon, Sung Ung | - |
dc.contributor.affiliatedAuthor | Park, Kyung Ah | - |
dc.contributor.affiliatedAuthor | Lee, Won Taek | - |
dc.contributor.affiliatedAuthor | Lee, Jong Eun | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 4 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1247 | - |
dc.citation.endPage | 1253 | - |
dc.identifier.bibliographicCitation | MOLECULAR MEDICINE REPORTS, Vol.4(6) : 1247-1253, 2011 | - |
dc.identifier.rimsid | 28615 | - |
dc.type.rims | ART | - |
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