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In vitro evidence of the role of COX-2 in attenuating gastric inflammation and promoting gastric carcinogenesis
DC Field | Value | Language |
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dc.contributor.author | Hahm, K.-B. | - |
dc.contributor.author | Lim, H.-Y. | - |
dc.contributor.author | Sohn, S. | - |
dc.contributor.author | Kwon, H.-J. | - |
dc.contributor.author | Lee, K.-M. | - |
dc.contributor.author | Lee, J.-S. | - |
dc.contributor.author | Surh, Y.-J. | - |
dc.contributor.author | Kim, Y.-B. | - |
dc.contributor.author | Joo, H.-J. | - |
dc.contributor.author | Kim, W.-S. | - |
dc.contributor.author | Cho, S.-W. | - |
dc.date.accessioned | 2023-03-28T02:40:12Z | - |
dc.date.available | 2023-03-28T02:40:12Z | - |
dc.date.created | 2020-12-10 | - |
dc.date.issued | 2002-02 | - |
dc.identifier.citation | Journal of Environmental Pathology, Toxicology and Oncology, Vol.21 No.2, pp.165-176 | - |
dc.identifier.issn | 0731-8898 | - |
dc.identifier.uri | https://hdl.handle.net/10371/189945 | - |
dc.description.abstract | Although gastric adenocarcinoma is one of the most common malignancies in the world, little is known about its exact molecular processes in development and progression. Recent studies suggest that COX-2 is important in carcinogenesis of gastrointestinal cancers, and is especially involved in carcinogenesis in a mouse model of familial adenomatosis polyposis. To understand the role of COX-2 in gastric carcinogenesis and Helicobacter pylori-associated gastritis, we measured COX-2 expression in 170 human gastric carcinoma tissues by immunohistochemical analysis and compared the expression of COX-2 in paired tissues obtained from normal-looking and cancer-bearing mucosa. Further evidence of the involvement of COX-2 in gastritis and gastric carcinogenesis was obtained by establishing stable cell lines overexpressing COX-2. After subcloning of COX-2 into pCB7 mammalian expression vector, two stable cell lines named MKN-28-COX-2 and MKN-45-COX-2 were generated by transfection of COX-2 cDNA. To understand the effect of COX-2 on gastritis, we performed an electrophoretic mobility shift assay of NF-κB (inflammation-associated transcription factor), and measured malondialdehyde levels and chemiluminescence activities in both mock-transfected MKN and MKN-COX-2 cells after stimulation of H. pylori (1 × 106 CFU/mL) and neutrophils (102 cells/mL). A marked attenuation of NF-κB bindings and generation of free radicals was observed in COX-2 overexpressed cells. Another set of experiments, including the growth inhibition by TGF-β treatment, Matrigel invasion assay, and apoptosis assay, was done. COX-2 showed the advantage of the escape from the growth inhibition by TGF-β through decreasing TGF-β RII expression and increased cell invasiveness. In conclusion, COX-2 expression seems to be induced to attenuate the degree of atrophic gastritis, the initial event in gastric carcinogenesis, and promote gastric carcinogenesis. | - |
dc.language | 영어 | - |
dc.publisher | Begell House | - |
dc.title | In vitro evidence of the role of COX-2 in attenuating gastric inflammation and promoting gastric carcinogenesis | - |
dc.type | Article | - |
dc.identifier.doi | 10.1615/JEnvironPatholToxicolOncol.v21.i2.100 | - |
dc.citation.journaltitle | Journal of Environmental Pathology, Toxicology and Oncology | - |
dc.identifier.scopusid | 2-s2.0-0036087711 | - |
dc.citation.endpage | 176 | - |
dc.citation.number | 2 | - |
dc.citation.startpage | 165 | - |
dc.citation.volume | 21 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Surh, Y.-J. | - |
dc.type.docType | Conference Paper | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | COX-2 | - |
dc.subject.keywordAuthor | Gastric carcinogenesis | - |
dc.subject.keywordAuthor | Helicobacter pylori | - |
dc.subject.keywordAuthor | MKN-28 | - |
dc.subject.keywordAuthor | MKN-45 | - |
dc.subject.keywordAuthor | Proliferation | - |
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