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Transcriptional silencing of Cyclooxygenase-2 by hyper-methylation of the 5′ CpG island in human gastric carcinoma cells
DC Field | Value | Language |
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dc.contributor.author | Song, Sang-Hyun | - |
dc.contributor.author | Jong, Hyun-Soon | - |
dc.contributor.author | Choi, Hyun Ho | - |
dc.contributor.author | Inoue, Hiroyasu | - |
dc.contributor.author | Tanabe, Tadashi | - |
dc.contributor.author | Kim, Noe Kyeong | - |
dc.contributor.author | Bang, Yung-Jue | - |
dc.date.accessioned | 2021-01-31T11:06:38Z | - |
dc.date.available | 2021-01-31T11:06:38Z | - |
dc.date.created | 2020-12-21 | - |
dc.date.issued | 2001-06 | - |
dc.identifier.citation | Cancer Research, Vol.61 No.11, pp.4628-4635 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.other | 119288 | - |
dc.identifier.uri | https://hdl.handle.net/10371/173030 | - |
dc.description.abstract | It has been well established that overexpression of Cyclooxygenase-2 (Cox-a) in epithetial cells inhibits apoptosis and increases the invasiveness of malignant cells, favoring tumorigenesis and metastasis, However, the molecular mechanism that regulates Cox-2 expression has not been well defined in gastric carcinoma. In this study, we examined whether the Cox-2 expression could be regulated by hyper-methylation of the Cox-2 CPG bland (spanning from -590 to +186 with respect to the transcription initiation site) in human gastric carcinoma cell lines. By Southern analysis, we found that three gastric cells (SNU-601, -620, and -719) without Cox-2 expression demonstrated hyper-methylation at the Cox-2 CpG island, A detailed methylation pattern using bisulfite sequencing analysis revealed that all of the CpG sites were completely methylated in SNU-601. Treatment with demethylating agents effectively reactivated the expression of Cox-2 and restored IL-1 beta sensitivity in the previously resistant SNU-601. By transient transfection experiments, we demonstrate that constitutively active Cox-2 promoter activities were exhibited even without an exogenous stimulation in SNU-601, Furthermore, when the motif of the nuclear factor for interleukin-6 expression site, the cyclic AMP response element, or both was subjected to point mutation, the constitutive luciferase activity was markedly reduced. In addition, Cox-2 promoter activity was completely blocked by irt vitro methylation of all of the CpG sites in the Cox-2 promoter region with SssI (CpG) methylase in SNU-601, Taken together, these results indicate that transcriptional repression of Cox-2 is caused by hyper-methylation of the Cox-2 CpG island in gastric carcinoma cell lines. | - |
dc.language | 영어 | - |
dc.publisher | American Association for Cancer Research | - |
dc.title | Transcriptional silencing of Cyclooxygenase-2 by hyper-methylation of the 5′ CpG island in human gastric carcinoma cells | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 방영주 | - |
dc.citation.journaltitle | Cancer Research | - |
dc.identifier.wosid | 000169051100054 | - |
dc.identifier.scopusid | 2-s2.0-0035360797 | - |
dc.citation.endpage | 4635 | - |
dc.citation.number | 11 | - |
dc.citation.startpage | 4628 | - |
dc.citation.volume | 61 | - |
dc.identifier.sci | 000169051100054 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Kim, Noe Kyeong | - |
dc.contributor.affiliatedAuthor | Bang, Yung-Jue | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | ENDOPEROXIDE SYNTHASE-2 GENE | - |
dc.subject.keywordPlus | PROTEIN-KINASE PATHWAYS | - |
dc.subject.keywordPlus | HUMAN COLON-CANCER | - |
dc.subject.keywordPlus | MICROSATELLITE INSTABILITY | - |
dc.subject.keywordPlus | DNA METHYLATION | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | COLORECTAL-CANCER | - |
dc.subject.keywordPlus | ENDOTHELIAL-CELLS | - |
dc.subject.keywordPlus | RESPONSE ELEMENT | - |
dc.subject.keywordPlus | MISMATCH REPAIR | - |
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