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Conference Paper: Role of cyclin D1 in conferring malignant phenotypes on immortalized esophageal epithelial cells

TitleRole of cyclin D1 in conferring malignant phenotypes on immortalized esophageal epithelial cells
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research
Citation
AACR 99th Annual Meeting, San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, Abstract no. 5581 How to Cite?
AbstractCyclin D1 is commonly overexpressed in many types of human squamous cell carcinomas, including esophageal squamous cell carcinoma. Studies in the past mainly focused on the role of cyclin D1 in cell growth and regulation of the G1/S transition of the cell cycle. Recently, malignant transformation induced by classical oncogenes was shown to be associated with upregulation of cyclin D1. So far, there are still no reports on the direct contribution of cyclin D1 to malignant transformation of immortalized epithelial cells. In this study, the role of cyclin D1 in the early stage of esophageal carcinogenesis was investigated by stable overexpression of cyclin D1 in an hTERT-immortalized esophageal epithelial cell line, NE2-hTERT. Our results showed that ectopic expression of cyclin D1 stimulated anchorage-independent growth in soft-agar, which is a major hallmark of transformed cells. This finding was further supported by the decrease in colony number in an esophageal cancer cell line (KYSE510) with cyclin D1 knockdown by siRNA. Cyclin D1 overexpressing esophageal epithelial cells also acquired a higher ability to migrate through cellular matrix, and showed reduced adhesion to different substrates. Western blotting and pull-down assays were used to further explore the mechanism involved. The results showed that the overexpression of cyclin D1 was associated with upregulation of pERK1/2 and reduced Rac1 activity. Our findings suggest that cyclin D1 overexpression promotes invasive potential and migration ability in immortalized esophageal epithelial cells, and that these malignant phenotypes may be mediated by pERK1/2 and cytoskeletal signaling. [This study is supported by the Research Grants Council of the Hong Kong SAR, China (Central allocation Project No. HKUST 2/06C)]
Persistent Identifierhttp://hdl.handle.net/10722/95560
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorCheung, PYen_HK
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorCheung, Aen_HK
dc.date.accessioned2010-09-25T16:06:06Z-
dc.date.available2010-09-25T16:06:06Z-
dc.date.issued2008en_HK
dc.identifier.citationAACR 99th Annual Meeting, San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, Abstract no. 5581en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95560-
dc.description.abstractCyclin D1 is commonly overexpressed in many types of human squamous cell carcinomas, including esophageal squamous cell carcinoma. Studies in the past mainly focused on the role of cyclin D1 in cell growth and regulation of the G1/S transition of the cell cycle. Recently, malignant transformation induced by classical oncogenes was shown to be associated with upregulation of cyclin D1. So far, there are still no reports on the direct contribution of cyclin D1 to malignant transformation of immortalized epithelial cells. In this study, the role of cyclin D1 in the early stage of esophageal carcinogenesis was investigated by stable overexpression of cyclin D1 in an hTERT-immortalized esophageal epithelial cell line, NE2-hTERT. Our results showed that ectopic expression of cyclin D1 stimulated anchorage-independent growth in soft-agar, which is a major hallmark of transformed cells. This finding was further supported by the decrease in colony number in an esophageal cancer cell line (KYSE510) with cyclin D1 knockdown by siRNA. Cyclin D1 overexpressing esophageal epithelial cells also acquired a higher ability to migrate through cellular matrix, and showed reduced adhesion to different substrates. Western blotting and pull-down assays were used to further explore the mechanism involved. The results showed that the overexpression of cyclin D1 was associated with upregulation of pERK1/2 and reduced Rac1 activity. Our findings suggest that cyclin D1 overexpression promotes invasive potential and migration ability in immortalized esophageal epithelial cells, and that these malignant phenotypes may be mediated by pERK1/2 and cytoskeletal signaling. [This study is supported by the Research Grants Council of the Hong Kong SAR, China (Central allocation Project No. HKUST 2/06C)]-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleRole of cyclin D1 in conferring malignant phenotypes on immortalized esophageal epithelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailCheung, A: lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.hkuros146542en_HK

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