Cited 14 times in
Cyclooxygenase inhibitors induce apoptosis in sinonasal cancer cells by increased expression of nonsteroidal anti-inflammatory drug-activated gene
DC Field | Value | Language |
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dc.contributor.author | 권순호 | - |
dc.contributor.author | 김경수 | - |
dc.contributor.author | 윤주헌 | - |
dc.date.accessioned | 2015-05-19T16:45:31Z | - |
dc.date.available | 2015-05-19T16:45:31Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 0020-7136 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/106890 | - |
dc.description.abstract | Nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) has recently been shown to be induced by nonsteroidal anti-inflammatory drugs (NSAIDs) and to have proapoptotic and antitumorigenic activities. Although sulindac sulfide induced apoptosis in sinonasal cancer cells, the relationship between NAG-1 and NSAIDs has not been determined. In this study, we investigated the induction of apoptosis in sinonasal cancer cells treated by various NSAIDs and the role of NAG-1 expression in this induction. The effect of NSAIDs on normal human nasal epithelial (NHNE) cells was also examined to evaluate their safety on normal cells. Finally, the in vivo anti-tumorigenic activity of NSAIDs in mice was investigated. In AMC-HN5 human sinonasal carcinoma cells, indomethacin was the most potent NAG-1 inducer and caused NAG-1 expression in a time- and dose-dependent manner. The induction of NAG-1 expression preceded the induction of apoptosis. Conditioned medium from NAG-1-overexpressing Drosophila cells inhibited proliferation of sinonasal cancer cells and induced apoptosis. In addition, in NAG-1 small interfering RNA-transfected cells, apoptosis induced by indomethacin was suppressed. In contrast, NAG-1 expression and apoptosis were not induced by NSAIDs or conditioned medium in NHNE cells. Furthermore, indomethacin induced a dose-dependent in vivo increase in the expression of NAG-1 mRNA in the mice tumors and the volume of xenograft tumors of AMC-HN5 cells in indomethacin-treated nude mice was reduced compared to that in control mice. In conclusion, indomethacin exerts proapoptotic and antitumorigenic effects in sinonasal cancer cells through the induction of NAG-1 and can be considered a safe and effective chemopreventive agent against sinonasal cancer | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1765~1773 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF CANCER | - |
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 | Animals | - |
dc.subject.MESH | Anti-Inflammatory Agents, Non-Steroidal/pharmacology* | - |
dc.subject.MESH | Antineoplastic Agents/pharmacology* | - |
dc.subject.MESH | Apoptosis/drug effects | - |
dc.subject.MESH | Blotting, Western | - |
dc.subject.MESH | Carcinoma/drug therapy* | - |
dc.subject.MESH | Carcinoma/metabolism | - |
dc.subject.MESH | Carcinoma/pathology | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cell Proliferation/drug effects | - |
dc.subject.MESH | Cyclooxygenase Inhibitors/pharmacology* | - |
dc.subject.MESH | Cytokines/drug effects | - |
dc.subject.MESH | Cytokines/genetics | - |
dc.subject.MESH | Cytokines/metabolism* | - |
dc.subject.MESH | Dose-Response Relationship, Drug | - |
dc.subject.MESH | Flow Cytometry | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic/drug effects | - |
dc.subject.MESH | Growth Differentiation Factor 15 | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Indomethacin/pharmacology* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Nude | - |
dc.subject.MESH | Paranasal Sinus Neoplasms/drug therapy* | - |
dc.subject.MESH | Paranasal Sinus Neoplasms/metabolism | - |
dc.subject.MESH | Paranasal Sinus Neoplasms/pathology | - |
dc.subject.MESH | RNA, Small Interfering | - |
dc.subject.MESH | Reverse Transcriptase Polymerase Chain Reaction | - |
dc.subject.MESH | Time Factors | - |
dc.subject.MESH | Transfection | - |
dc.subject.MESH | Up-Regulation | - |
dc.title | Cyclooxygenase inhibitors induce apoptosis in sinonasal cancer cells by increased expression of nonsteroidal anti-inflammatory drug-activated gene | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Otorhinolaryngology (이비인후과학) | - |
dc.contributor.googleauthor | Jeong Hong Kim | - |
dc.contributor.googleauthor | Jung Hyun Chang | - |
dc.contributor.googleauthor | Kwang-Hyeon Rhee | - |
dc.contributor.googleauthor | Joo-Heon Yoon | - |
dc.contributor.googleauthor | Soon Ho Kwon | - |
dc.contributor.googleauthor | Keejae Song | - |
dc.contributor.googleauthor | Kun Wayn Lee | - |
dc.contributor.googleauthor | Chang Il Cho | - |
dc.contributor.googleauthor | Ju Hyun Jeon | - |
dc.contributor.googleauthor | Kyung-Su Kim | - |
dc.identifier.doi | 10.1002/ijc.23302 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00223 | - |
dc.contributor.localId | A00298 | - |
dc.contributor.localId | A02604 | - |
dc.relation.journalcode | J01092 | - |
dc.identifier.eissn | 1097-0215 | - |
dc.identifier.pmid | 18076062 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1002/ijc.23302/abstract | - |
dc.subject.keyword | NSAIDs | - |
dc.subject.keyword | NAG‐1 | - |
dc.subject.keyword | sinonasal cancer | - |
dc.subject.keyword | chemoprevention | - |
dc.contributor.alternativeName | Kwon, Soon Ho | - |
dc.contributor.alternativeName | Kim, Kyung Su | - |
dc.contributor.alternativeName | Yoon, Joo Heon | - |
dc.contributor.affiliatedAuthor | Kwon, Soon Ho | - |
dc.contributor.affiliatedAuthor | Kim, Kyung Su | - |
dc.contributor.affiliatedAuthor | Yoon, Joo Heon | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 122 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 1765 | - |
dc.citation.endPage | 1773 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF CANCER, Vol.122(8) : 1765-1773, 2008 | - |
dc.identifier.rimsid | 50918 | - |
dc.type.rims | ART | - |
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