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Article: Role of p14ARF in TWIST-mediated senescence in prostate epithelial cells

TitleRole of p14ARF in TWIST-mediated senescence in prostate epithelial cells
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2007, v. 28 n. 12, p. 2467-2475 How to Cite?
AbstractRecently, TWIST, a basic helix-loop-helix transcription factor, is suggested to be an oncogene because of its over-expression in many types of human cancer and its positive role in promoting cell survival. The aim of this study was to investigate the role of TWIST on the growth of human epithelial cells. Using two immortalized human prostate epithelial cell lines, we demonstrated that inactivation of TWIST by small RNA technology led to the promotion of cellular senescence and growth arrest, suggesting that TWIST plays a key role in the continuous proliferation of immortalized cells. Over-expression of TWIST, in contrast, resulted in suppression of cellular senescence in response to genotoxic damage and promotion of cell proliferation with DNA damage accumulation, indicating that TWIST promotes genomic instability. In addition, we also found that the TWIST-mediated cellular senescence was regulated through its negative effect on p14ARF and subsequent suppression of MDM2/p53 and Chk1/2 DNA damage response pathways. Our results suggest that over-expression of TWIST results in down-regulation of p14ARF, which leads to the impairment of DNA damage checkpoint in response to genotoxic stress. This negative effect of TWIST on DNA damage response facilitates uncontrolled cell proliferation with genomic instability and tumorigenesis in non-malignant cells. © The Author 2007. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67789
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwok, WKen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorYuen, HFen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:58:16Z-
dc.date.available2010-09-06T05:58:16Z-
dc.date.issued2007en_HK
dc.identifier.citationCarcinogenesis, 2007, v. 28 n. 12, p. 2467-2475en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67789-
dc.description.abstractRecently, TWIST, a basic helix-loop-helix transcription factor, is suggested to be an oncogene because of its over-expression in many types of human cancer and its positive role in promoting cell survival. The aim of this study was to investigate the role of TWIST on the growth of human epithelial cells. Using two immortalized human prostate epithelial cell lines, we demonstrated that inactivation of TWIST by small RNA technology led to the promotion of cellular senescence and growth arrest, suggesting that TWIST plays a key role in the continuous proliferation of immortalized cells. Over-expression of TWIST, in contrast, resulted in suppression of cellular senescence in response to genotoxic damage and promotion of cell proliferation with DNA damage accumulation, indicating that TWIST promotes genomic instability. In addition, we also found that the TWIST-mediated cellular senescence was regulated through its negative effect on p14ARF and subsequent suppression of MDM2/p53 and Chk1/2 DNA damage response pathways. Our results suggest that over-expression of TWIST results in down-regulation of p14ARF, which leads to the impairment of DNA damage checkpoint in response to genotoxic stress. This negative effect of TWIST on DNA damage response facilitates uncontrolled cell proliferation with genomic instability and tumorigenesis in non-malignant cells. © The Author 2007. Published by Oxford University Press. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshCell Aging - physiologyen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshDNA Damage - physiologyen_HK
dc.subject.meshEpithelial Cells - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNuclear Proteins - physiologyen_HK
dc.subject.meshProstate - cytologyen_HK
dc.subject.meshProtein Kinases - metabolismen_HK
dc.subject.meshProtein-Serine-Threonine Kinases - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-mdm2 - metabolismen_HK
dc.subject.meshTumor Suppressor Protein p14ARF - physiologyen_HK
dc.subject.meshTumor Suppressor Protein p53 - metabolismen_HK
dc.subject.meshTwist Transcription Factor - physiologyen_HK
dc.titleRole of p14ARF in TWIST-mediated senescence in prostate epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=28&issue=12&spage=2467&epage=2475&date=2007&atitle=Role+of+p14ARF+in+TWIST-mediated+senescence+in+prostate+epithelial+cellsen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/carcin/bgm185en_HK
dc.identifier.pmid17690110-
dc.identifier.scopuseid_2-s2.0-36949002825en_HK
dc.identifier.hkuros147769en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-36949002825&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue12en_HK
dc.identifier.spage2467en_HK
dc.identifier.epage2475en_HK
dc.identifier.isiWOS:000251505800006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKwok, WK=8578541800en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridYuen, HF=14018633400en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK

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