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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 FieldValueLanguage
dc.contributor.author김귀언-
dc.contributor.author서창옥-
dc.date.accessioned2017-10-26T06:35:38Z-
dc.date.available2017-10-26T06:35:38Z-
dc.date.issued2005-
dc.identifier.issn0008-5472-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/151055-
dc.description.abstractTo 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.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherAmerican Association for Cancer Research-
dc.relation.isPartOfCANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleRadiosensitivity 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.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Radiation Oncology (방사선종양학교실)-
dc.contributor.departmentDept. of Radiation Oncology (방사선종양학교실)-
dc.contributor.googleauthorYou Keun Shin-
dc.contributor.googleauthorJi Sun Park-
dc.contributor.googleauthorHyun Seok Kim-
dc.contributor.googleauthorHyun Jung Jun-
dc.contributor.googleauthorGwi Eon Kim-
dc.contributor.googleauthorChang Ok Suh-
dc.contributor.googleauthorYeon Sook Yun-
dc.contributor.googleauthorHongryull Pyo-
dc.identifier.doi10.1158/0008-5472.CAN-05-0220-
dc.contributor.localIdA00321-
dc.contributor.localIdA01919-
dc.relation.journalcodeJ00452-
dc.identifier.eissn1538-7445-
dc.identifier.pmid10.1158/0008-5472.CAN-05-0220-
dc.contributor.alternativeNameKim, Gwi Eon-
dc.contributor.alternativeNameSuh, Chang Ok-
dc.citation.volume65-
dc.citation.number20-
dc.citation.startPage9501-
dc.citation.endPage9509-
dc.identifier.bibliographicCitationCANCER RESEARCH, Vol.65(20) : 9501-9509, 2005-
dc.date.modified2017-05-04-
dc.identifier.rimsid43403-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers

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