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Article: Early upregulation of cyclooxygenase-2 in human papillomavirus type 16 and telomerase-induced immortalization of human esophageal epithelial cells

TitleEarly upregulation of cyclooxygenase-2 in human papillomavirus type 16 and telomerase-induced immortalization of human esophageal epithelial cells
Authors
KeywordsCell cycle
Cyclooxygenase-2
Esophageal cancer
Immortalization
Telomerase
Issue Date2008
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
Journal Of Gastroenterology And Hepatology, 2008, v. 23 n. 10, p. 1613-1620 How to Cite?
AbstractBackground and Aim: Cyclooxygenase-2 (COX-2) plays an important role in the carcinogenesis of esophageal squamous cell carcinoma (ESCC). However, it is not clear whether COX-2 is involved in the early or late stage of the development of ESCC. The aim of this study was to investigate the role of COX-2 in the carcinogenesis of ESCC by an immortalized esophageal epithelial cell line. Methods: Human papillomavirus type 16 (HPV16)-E6/E7 and human telomerase reverse transcriptase (hTERT) transfection were used for immortalization of esophageal epithelial cells. COX-2-specific RNA interference was used for the inhibition of COX-2 expression. Results: An immortalized esophageal epithelial cell line, NE6-E6E7/hTERT, was established, which had high proliferation activity but failed to induce colony formation in soft agar. COX-2 expression was upregulated in the early process of immortalization, while COX-2 small interfering RNA (siRNA) decreased the Bcl-2 expression, increased the expression of Bax, and induced cell-cycle arrest at the G0/G1 phase in NE6-E6E7/hTERT cells. Expressions of p53, cyclinD1, and the ratio of hyperphosphorylated-RB/ hypophosphorylated-RB were progressively increased after E6E7 and the subsequent hTERT transfections. These changes were accompanied by the alteration of COX-2 expression, but could be reversed by COX-2 siRNA (P < 0.05). P16 expression was significantly downregulated in NE6-E6E7 or NE6-E6E7/hTERT cells (P < 0.05), and was not affected by COX-2 siRNA. Conclusions: Our results suggest that induction of cyclooxygenase-2 is essential in the human papillomavirus type 16 and hTERT-induced immortalization of human esophageal epithelial cells, and that COX-2 inhibition may be a potential target to block the carcinogenesis of ESCC at the precancerous stage. © 2008 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/58197
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190
ISI Accession Number ID
Funding AgencyGrant Number
Gastroenterological Research Fund
University of Hong Kong, Hong Kong
Funding Information:

This study was supported by the Gastroenterological Research Fund, University of Hong Kong, Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorZhuang, ZHen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorWang, JDen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorHe, Hen_HK
dc.contributor.authorFeng, HCen_HK
dc.contributor.authorWang, LDen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-05-31T03:25:39Z-
dc.date.available2010-05-31T03:25:39Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Gastroenterology And Hepatology, 2008, v. 23 n. 10, p. 1613-1620en_HK
dc.identifier.issn0815-9319en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58197-
dc.description.abstractBackground and Aim: Cyclooxygenase-2 (COX-2) plays an important role in the carcinogenesis of esophageal squamous cell carcinoma (ESCC). However, it is not clear whether COX-2 is involved in the early or late stage of the development of ESCC. The aim of this study was to investigate the role of COX-2 in the carcinogenesis of ESCC by an immortalized esophageal epithelial cell line. Methods: Human papillomavirus type 16 (HPV16)-E6/E7 and human telomerase reverse transcriptase (hTERT) transfection were used for immortalization of esophageal epithelial cells. COX-2-specific RNA interference was used for the inhibition of COX-2 expression. Results: An immortalized esophageal epithelial cell line, NE6-E6E7/hTERT, was established, which had high proliferation activity but failed to induce colony formation in soft agar. COX-2 expression was upregulated in the early process of immortalization, while COX-2 small interfering RNA (siRNA) decreased the Bcl-2 expression, increased the expression of Bax, and induced cell-cycle arrest at the G0/G1 phase in NE6-E6E7/hTERT cells. Expressions of p53, cyclinD1, and the ratio of hyperphosphorylated-RB/ hypophosphorylated-RB were progressively increased after E6E7 and the subsequent hTERT transfections. These changes were accompanied by the alteration of COX-2 expression, but could be reversed by COX-2 siRNA (P < 0.05). P16 expression was significantly downregulated in NE6-E6E7 or NE6-E6E7/hTERT cells (P < 0.05), and was not affected by COX-2 siRNA. Conclusions: Our results suggest that induction of cyclooxygenase-2 is essential in the human papillomavirus type 16 and hTERT-induced immortalization of human esophageal epithelial cells, and that COX-2 inhibition may be a potential target to block the carcinogenesis of ESCC at the precancerous stage. © 2008 The Authors.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGHen_HK
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_HK
dc.subjectCell cycleen_HK
dc.subjectCyclooxygenase-2en_HK
dc.subjectEsophageal canceren_HK
dc.subjectImmortalizationen_HK
dc.subjectTelomeraseen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCell Cycleen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolism - pathologyen_HK
dc.subject.meshCell Transformation, Viralen_HK
dc.subject.meshCyclooxygenase 2 - genetics - metabolismen_HK
dc.subject.meshDinoprostone - metabolismen_HK
dc.subject.meshEpithelial Cells - enzymology - pathology - virologyen_HK
dc.subject.meshEsophagus - enzymology - pathology - virologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshKaryotypingen_HK
dc.subject.meshNeoplastic Stem Cells - enzymologyen_HK
dc.subject.meshOncogene Proteins, Viral - genetics - metabolismen_HK
dc.subject.meshPapillomavirus E7 Proteinsen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA, Small Interfering - metabolismen_HK
dc.subject.meshRepressor Proteins - genetics - metabolismen_HK
dc.subject.meshRetinoblastoma Protein - metabolismen_HK
dc.subject.meshTelomerase - genetics - metabolismen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Suppressor Protein p53 - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshbcl-2-Associated X Protein - metabolismen_HK
dc.titleEarly upregulation of cyclooxygenase-2 in human papillomavirus type 16 and telomerase-induced immortalization of human esophageal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0815-9319&volume=23&spage=1613&epage=1620&date=2008&atitle=Early+Upregulation+of+Cyclooxygenase-2+in+Human+Papillomavirus+Type+16+and+Telomerase-induced+Immortalization+of+Human+Esophageal+Epithelial+Cellsen_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.emailWang, JD: jidewang@gmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.identifier.authorityWang, JD=rp00491en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1746.2008.05509.xen_HK
dc.identifier.pmid18717758-
dc.identifier.scopuseid_2-s2.0-53349101676en_HK
dc.identifier.hkuros150132en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-53349101676&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1613en_HK
dc.identifier.epage1620en_HK
dc.identifier.isiWOS:000259815300025-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridZhuang, ZH=7203003327en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK
dc.identifier.scopusauthoridWang, JD=35309087500en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridHe, H=36185495900en_HK
dc.identifier.scopusauthoridFeng, HC=7401736336en_HK
dc.identifier.scopusauthoridWang, LD=12242861000en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridLam, SK=7402279800en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.citeulike3389163-

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