Cited 94 times in
Radiosensitivity enhancement by celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, via COX-2-dependent cell cycle regulation on human cancer cells expressing differential COX-2 levels
DC Field | Value | Language |
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dc.contributor.author | 김귀언 | - |
dc.contributor.author | 서창옥 | - |
dc.date.accessioned | 2017-10-26T06:35:38Z | - |
dc.date.available | 2017-10-26T06:35:38Z | - |
dc.date.issued | 2005 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/151055 | - |
dc.description.abstract | To characterize the radiation-enhancing effects on human cancer cells and underlying mechanisms of celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, and to ascertain whether its effects are COX-2 dependent. Clonogenic cytotoxicity assays and radiation survival assays after treatment with celecoxib ± radiation were done on four human cancer cell lines that expressed differential COX-2 levels. Stably COX-2 knocked down or overexpressed cell lines were developed, and clonogenic assays, apoptosis assays, or cell cycle change measurements were conducted after treatment with celecoxib ± radiation. Prostaglandin E2 (PGE2) was applied to medium after treatment with celecoxib ± radiation to determine whether the radiation-enhancing effect associated with celecoxib results from reduced generation of prostaglandin. Celecoxib's radiation-enhancing effect was observed in COX-2–expressing A549 and NCI-H460 cells but was not observed in the COX-2 nonexpressing MCF-7 and HCT-116 cells. Celecoxib's radiation-enhancing effects in A549 cells were shown to disappear after the administration of COX-2 knocked down. In contrast, the HCT-116 cells were radiosensitized by celecoxib after being transfected with COX-2 expression vector. The addition of PGE2 after treatment with celecoxib ± radiation had no significant effects on celecoxib's radiation-enhancing effects in A549 and COX-2 transfected HCT-116 cells. Radiation-induced G2-M arrest was enhanced and sustained in the COX-2–overexpressing cells compared with that seen in COX-2 low-expressing cells. Celecoxib or NS-398 effected no changes or attenuated radiation-induced G2-M arrest in the COX-2–overexpressing cells but further enhanced the radiation-induced G2-M arrest in the COX-2 low-expressing cells. Celecoxib's radiation-enhancing effects seem to occur in a COX-2 expression-dependent manner in the cancer cells. This effect does not seem to be the result of reduced PGE2 generation. Celecoxib may exert an inhibitory effect on enhanced radiation-induced G2-M arrest in the COX-2–overexpressing cells, which may allow the arrested cells to enter mitosis and die after radiation, but may also further enhance radiation-induced G2-M arrest in the COX-2 low-expressing cells, by virtue of another mechanism. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | American Association for Cancer Research | - |
dc.relation.isPartOf | CANCER RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Radiosensitivity enhancement by celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, via COX-2-dependent cell cycle regulation on human cancer cells expressing differential COX-2 levels | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Radiation Oncology (방사선종양학교실) | - |
dc.contributor.department | Dept. of Radiation Oncology (방사선종양학교실) | - |
dc.contributor.googleauthor | You Keun Shin | - |
dc.contributor.googleauthor | Ji Sun Park | - |
dc.contributor.googleauthor | Hyun Seok Kim | - |
dc.contributor.googleauthor | Hyun Jung Jun | - |
dc.contributor.googleauthor | Gwi Eon Kim | - |
dc.contributor.googleauthor | Chang Ok Suh | - |
dc.contributor.googleauthor | Yeon Sook Yun | - |
dc.contributor.googleauthor | Hongryull Pyo | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-05-0220 | - |
dc.contributor.localId | A00321 | - |
dc.contributor.localId | A01919 | - |
dc.relation.journalcode | J00452 | - |
dc.identifier.eissn | 1538-7445 | - |
dc.identifier.pmid | 10.1158/0008-5472.CAN-05-0220 | - |
dc.contributor.alternativeName | Kim, Gwi Eon | - |
dc.contributor.alternativeName | Suh, Chang Ok | - |
dc.citation.volume | 65 | - |
dc.citation.number | 20 | - |
dc.citation.startPage | 9501 | - |
dc.citation.endPage | 9509 | - |
dc.identifier.bibliographicCitation | CANCER RESEARCH, Vol.65(20) : 9501-9509, 2005 | - |
dc.date.modified | 2017-05-04 | - |
dc.identifier.rimsid | 43403 | - |
dc.type.rims | ART | - |
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