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Article: The multistage process of carcinogenesis in human esophageal epithelial cells induced by human papillomavirus.

TitleThe multistage process of carcinogenesis in human esophageal epithelial cells induced by human papillomavirus.
Authors
Issue Date2004
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
Citation
Oncology Reports, 2004, v. 11 n. 3, p. 647-654 How to Cite?
AbstractTo investigate the multistage process of carcinogenesis, the progressive alteration of the morphology, telomerase, cytogenesis, oncogenes and tumorigenicity in the process of immortalization and malignant transformation of the human fetal esophageal epithelial cell (SHEE) was studied. The SHEE cells were immortalized by gene E6E7 of human papilloma virus (HPV) type 18 in our laboratory and continually cultivated over 100 passages, which had been malignantly transformed. Cells at the 11th, 35th, 65th and 100th passage were examined according to the following criteria: morphological changes of cell growth, contact-inhibition and anchorage-independent growth (AIG); the cell proliferative and apoptotic index; the modal number of chromosomes; c-myc, p53, bcl-2, ras; telomere length and activities of telomerase and tumorigenicity in nude mice or severe combined immunodeficient (SCID) mice. The cells of the 11th passage were well differentiated and the cells of 100th passage were relatively poorly differentiated with polymorphism, while the cells of 35th and 65th had two distinct differentiations. The proliferative indexes were 21.1%, 32.5%, 33.2%, and 40.9% and the apoptotic indexes were 3.3%, 2.7%, 3.5%, 2.7% in the 11th, 35th, 65th and 100th passage respectively. Karyotypes of four cell passages belonged to hyperdiploidy and hypotriploidy. C-myc, ras, p53 genes were low in the 10th and 35th, and high in the 65th and 100th passage, but bcl-2 was low in 4 passages. Telomere length sharply decreased from normal fetal esophagus cells until the 35th passage, but it was stably expressed in the 65th and 100th passage. The activities of telomerase were expressed in cells of the 35th, 65th and 100th passages. The efficiency of AIG varied in different passages of the SHEE cell and was absent in the 11th passage, low efficiency in the 35th passage and 65th passage, and high efficiency in the 100th passage. Transplanted cells of the 65th and 100th passage into SCID mice resulted in tumor formation, but only the 100th passage cells could grow in nude mice. All of these characteristic changes were in dynamic progressive process. These data demonstrate that carcinogenesis of esophageal epithelial cells induced by HPV is the multistage process, which goes through the initial, immortal, premalignant and malignant transformation stages. The generation of esophageal carcinoma is caused by the accumulation of cellular, genetic and molecular changes.
Persistent Identifierhttp://hdl.handle.net/10722/149698
ISSN
2015 Impact Factor: 2.486
2015 SCImago Journal Rankings: 0.968
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShen, ZYen_US
dc.contributor.authorXu, LYen_US
dc.contributor.authorLi, EMen_US
dc.contributor.authorCai, WJen_US
dc.contributor.authorShen, Jen_US
dc.contributor.authorChen, MHen_US
dc.contributor.authorCen, Sen_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorZeng, Yen_US
dc.date.accessioned2012-06-26T05:57:16Z-
dc.date.available2012-06-26T05:57:16Z-
dc.date.issued2004en_US
dc.identifier.citationOncology Reports, 2004, v. 11 n. 3, p. 647-654en_US
dc.identifier.issn1021-335Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/149698-
dc.description.abstractTo investigate the multistage process of carcinogenesis, the progressive alteration of the morphology, telomerase, cytogenesis, oncogenes and tumorigenicity in the process of immortalization and malignant transformation of the human fetal esophageal epithelial cell (SHEE) was studied. The SHEE cells were immortalized by gene E6E7 of human papilloma virus (HPV) type 18 in our laboratory and continually cultivated over 100 passages, which had been malignantly transformed. Cells at the 11th, 35th, 65th and 100th passage were examined according to the following criteria: morphological changes of cell growth, contact-inhibition and anchorage-independent growth (AIG); the cell proliferative and apoptotic index; the modal number of chromosomes; c-myc, p53, bcl-2, ras; telomere length and activities of telomerase and tumorigenicity in nude mice or severe combined immunodeficient (SCID) mice. The cells of the 11th passage were well differentiated and the cells of 100th passage were relatively poorly differentiated with polymorphism, while the cells of 35th and 65th had two distinct differentiations. The proliferative indexes were 21.1%, 32.5%, 33.2%, and 40.9% and the apoptotic indexes were 3.3%, 2.7%, 3.5%, 2.7% in the 11th, 35th, 65th and 100th passage respectively. Karyotypes of four cell passages belonged to hyperdiploidy and hypotriploidy. C-myc, ras, p53 genes were low in the 10th and 35th, and high in the 65th and 100th passage, but bcl-2 was low in 4 passages. Telomere length sharply decreased from normal fetal esophagus cells until the 35th passage, but it was stably expressed in the 65th and 100th passage. The activities of telomerase were expressed in cells of the 35th, 65th and 100th passages. The efficiency of AIG varied in different passages of the SHEE cell and was absent in the 11th passage, low efficiency in the 35th passage and 65th passage, and high efficiency in the 100th passage. Transplanted cells of the 65th and 100th passage into SCID mice resulted in tumor formation, but only the 100th passage cells could grow in nude mice. All of these characteristic changes were in dynamic progressive process. These data demonstrate that carcinogenesis of esophageal epithelial cells induced by HPV is the multistage process, which goes through the initial, immortal, premalignant and malignant transformation stages. The generation of esophageal carcinoma is caused by the accumulation of cellular, genetic and molecular changes.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htmen_US
dc.relation.ispartofOncology reportsen_US
dc.subject.meshAgar - Chemistry - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Cycleen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Transformation, Neoplasticen_US
dc.subject.meshEpithelial Cells - Pathology - Virologyen_US
dc.subject.meshEsophageal Neoplasms - Pathology - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshMice, Sciden_US
dc.subject.meshMicroscopy, Phase-Contrasten_US
dc.subject.meshNeoplasm Transplantationen_US
dc.subject.meshPapillomaviridae - Metabolismen_US
dc.subject.meshPloidiesen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Myc - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshTelomerase - Metabolismen_US
dc.subject.meshTelomere - Ultrastructureen_US
dc.subject.meshTime Factorsen_US
dc.titleThe multistage process of carcinogenesis in human esophageal epithelial cells induced by human papillomavirus.en_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.pmid14767516-
dc.identifier.scopuseid_2-s2.0-4644371692en_US
dc.identifier.hkuros95022-
dc.identifier.volume11en_US
dc.identifier.issue3en_US
dc.identifier.spage647en_US
dc.identifier.epage654en_US
dc.identifier.isiWOS:000188964900009-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridShen, ZY=7403324731en_US
dc.identifier.scopusauthoridXu, LY=7404744339en_US
dc.identifier.scopusauthoridLi, EM=7201410160en_US
dc.identifier.scopusauthoridCai, WJ=7401711109en_US
dc.identifier.scopusauthoridShen, J=37110196900en_US
dc.identifier.scopusauthoridChen, MH=7406353285en_US
dc.identifier.scopusauthoridCen, S=55041274600en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridZeng, Y=22973861100en_US

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