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Article: Cyclooxygenase-2 expression in esophageal cancer cells and induction by mitomycin C

TitleCyclooxygenase-2 expression in esophageal cancer cells and induction by mitomycin C
Authors
Issue Date2003
Citation
Zhonghua Nei Ke Za Zhi [Chinese Journal Of Internal Medicine], 2003, v. 42 n. 10, p. 701-704 How to Cite?
AbstractOBJECTIVE: To study the relationship between COX-2 expression in esophageal cancer cell (EC/CUHK-1) and mitomycin C (MMC) treatment. METHODS: 2 mg/L of MMC was added to the well-grown EC/CUHK-1 cells cultured in RPMI-1640 including 10% FCS, and the medium was totally changed after 0.5, 1, 2, 4 and 8 h treatment, respectively. Cells were collected after another 24 h culture. Protein expression of COX-2, Bcl-2, Rb, p53 were examined by Western blot, and RT-PCR method was used to confirm the COX-2 expression in mRNA level. Cell cycle analysis for cells collected at 0, 0.5, 2, 4 and 8 h was performed on an EPICS profile analyzer. RESULTS: The cell cycle analysis showed that the percentage of apoptosis cells were (4.12 +/- 0.83)%, (1.00 +/- 0.11)%, (4.32 +/- 0.99)%, (9.46 +/- 2.11)% and (31.10 +/- 3.57)%, respectively. COX-2 mRNA expression were 2.60, 1.70, and 0.08 times, COX-2 protein expression were 2.0, 3.1 and 2.8 times, Bcl-2 protein were 3.6, 14.0 and 12.0 times, p53 protein were 1.8, 0.5 and 0.2 times, hyperphosphorylated form Rb were 8.2, 8.4 and 6.2 times, underphosphorylated form Rb were 1.8, 0.5 and 0.2 times in 0.5, 2 and 4 h after MMC treatment, respectively, as compared with the control group. CONCLUSIONS: The COX-2 expression showed coincidence up-regulation according to the MMC-induced anti-apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation. It is implied that COX-2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX-2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable.
Persistent Identifierhttp://hdl.handle.net/10722/149630
ISSN
2015 SCImago Journal Rankings: 0.150

 

DC FieldValueLanguage
dc.contributor.authorZhuang, ZHen_US
dc.contributor.authorWang, LDen_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorCheung, LMen_US
dc.contributor.authorFeng, HCen_US
dc.contributor.authorYang, Ten_US
dc.contributor.authorQin, YRen_US
dc.contributor.authorWang, CDen_US
dc.contributor.authorChen, ZZen_US
dc.contributor.authorLiu, Ben_US
dc.date.accessioned2012-06-26T05:56:16Z-
dc.date.available2012-06-26T05:56:16Z-
dc.date.issued2003en_US
dc.identifier.citationZhonghua Nei Ke Za Zhi [Chinese Journal Of Internal Medicine], 2003, v. 42 n. 10, p. 701-704en_US
dc.identifier.issn0578-1426en_US
dc.identifier.urihttp://hdl.handle.net/10722/149630-
dc.description.abstractOBJECTIVE: To study the relationship between COX-2 expression in esophageal cancer cell (EC/CUHK-1) and mitomycin C (MMC) treatment. METHODS: 2 mg/L of MMC was added to the well-grown EC/CUHK-1 cells cultured in RPMI-1640 including 10% FCS, and the medium was totally changed after 0.5, 1, 2, 4 and 8 h treatment, respectively. Cells were collected after another 24 h culture. Protein expression of COX-2, Bcl-2, Rb, p53 were examined by Western blot, and RT-PCR method was used to confirm the COX-2 expression in mRNA level. Cell cycle analysis for cells collected at 0, 0.5, 2, 4 and 8 h was performed on an EPICS profile analyzer. RESULTS: The cell cycle analysis showed that the percentage of apoptosis cells were (4.12 +/- 0.83)%, (1.00 +/- 0.11)%, (4.32 +/- 0.99)%, (9.46 +/- 2.11)% and (31.10 +/- 3.57)%, respectively. COX-2 mRNA expression were 2.60, 1.70, and 0.08 times, COX-2 protein expression were 2.0, 3.1 and 2.8 times, Bcl-2 protein were 3.6, 14.0 and 12.0 times, p53 protein were 1.8, 0.5 and 0.2 times, hyperphosphorylated form Rb were 8.2, 8.4 and 6.2 times, underphosphorylated form Rb were 1.8, 0.5 and 0.2 times in 0.5, 2 and 4 h after MMC treatment, respectively, as compared with the control group. CONCLUSIONS: The COX-2 expression showed coincidence up-regulation according to the MMC-induced anti-apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation. It is implied that COX-2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX-2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable.en_US
dc.languageengen_US
dc.relation.ispartofZhonghua nei ke za zhi [Chinese journal of internal medicine]en_US
dc.subject.meshAntibiotics, Antineoplastic - Pharmacologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshEsophageal Neoplasms - Enzymology - Pathologyen_US
dc.subject.meshGene Expression Regulation, Enzymologic - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshIsoenzymes - Genetics - Metabolismen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshMitomycin - Pharmacologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Genetics - Metabolismen_US
dc.subject.meshRna, Messenger - Drug Effects - Metabolismen_US
dc.subject.meshRetinoblastoma Protein - Metabolismen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTumor Suppressor Protein P53 - Metabolismen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.titleCyclooxygenase-2 expression in esophageal cancer cells and induction by mitomycin Cen_US
dc.typeArticleen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid14633464-
dc.identifier.scopuseid_2-s2.0-1542543464en_US
dc.identifier.hkuros95019-
dc.identifier.volume42en_US
dc.identifier.issue10en_US
dc.identifier.spage701en_US
dc.identifier.epage704en_US
dc.identifier.scopusauthoridZhuang, ZH=7203003327en_US
dc.identifier.scopusauthoridWang, LD=12242861000en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridCheung, LM=7102302748en_US
dc.identifier.scopusauthoridFeng, HC=7401736336en_US
dc.identifier.scopusauthoridYang, T=8966950300en_US
dc.identifier.scopusauthoridQin, YR=7403100680en_US
dc.identifier.scopusauthoridWang, CD=9942133500en_US
dc.identifier.scopusauthoridChen, ZZ=7409484491en_US
dc.identifier.scopusauthoridLiu, B=7408693699en_US

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