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Article: Transcriptional repression of WEE1 by Kruppel-like factor 2 is involved in DNA damage-induced apoptosis

TitleTranscriptional repression of WEE1 by Kruppel-like factor 2 is involved in DNA damage-induced apoptosis
Authors
KeywordsKLF2
Transcriptional regulation
WEE1
Issue Date2005
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2005, v. 24 n. 24, p. 3875-3885 How to Cite?
AbstractHuman Kruppel-like factor 2 (KLF2) is a Cys 2/His 2 zinc-finger-containing transcriptional factor, which is involved in multiple cellular pathways. Utilizing gene expression profiling to identify aberrantly expressed genes in ovarian cancer, we found that KLF2 was significantly and specifically downregulated in ovarian tumors. After reintroducing KLF2 into ovarian cancer cell lines, we observed decreased cell growth and increased sensitivity to DNA damage-induced apoptosis. Analysis of genes that could be potential targets of KLF2 revealed that KLF2 negatively regulated WEE1 expression. WEE1 encodes a tyrosine kinase that regulates the G2/M cell cycle transition. Expression of KLF2 markedly repressed the transcription of WEE1 by directly binding to an SP1/CPBP motif located between -252bp and the start codon of the WEE1 promoter. Both activation and zinc-finger domains of KLF2 were required for this suppression of Wee1 expression. In addition, we demonstrated that Wee1 expression prevents cancer cells from undergoing apoptosis in response to DNA damage; however, this resistance was abolished by coexpression of KLF2, which inhibits WEE1 transcription. Thus, the level of WEE1 is regulated by KLF2 and enhanced KLF2 expression sensitizes cells to DNA damage-induced apoptosis. © 2005 Nature Publishing Group. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87148
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Fen_HK
dc.contributor.authorZhu, Yen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorMcAvoy, Sen_HK
dc.contributor.authorJohnson, WBen_HK
dc.contributor.authorCheung, THen_HK
dc.contributor.authorChung, TKHen_HK
dc.contributor.authorLo, KWKen_HK
dc.contributor.authorYim, SFen_HK
dc.contributor.authorYu, MMYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorWong, YFen_HK
dc.contributor.authorSmith, DIen_HK
dc.date.accessioned2010-09-06T09:25:57Z-
dc.date.available2010-09-06T09:25:57Z-
dc.date.issued2005en_HK
dc.identifier.citationOncogene, 2005, v. 24 n. 24, p. 3875-3885en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87148-
dc.description.abstractHuman Kruppel-like factor 2 (KLF2) is a Cys 2/His 2 zinc-finger-containing transcriptional factor, which is involved in multiple cellular pathways. Utilizing gene expression profiling to identify aberrantly expressed genes in ovarian cancer, we found that KLF2 was significantly and specifically downregulated in ovarian tumors. After reintroducing KLF2 into ovarian cancer cell lines, we observed decreased cell growth and increased sensitivity to DNA damage-induced apoptosis. Analysis of genes that could be potential targets of KLF2 revealed that KLF2 negatively regulated WEE1 expression. WEE1 encodes a tyrosine kinase that regulates the G2/M cell cycle transition. Expression of KLF2 markedly repressed the transcription of WEE1 by directly binding to an SP1/CPBP motif located between -252bp and the start codon of the WEE1 promoter. Both activation and zinc-finger domains of KLF2 were required for this suppression of Wee1 expression. In addition, we demonstrated that Wee1 expression prevents cancer cells from undergoing apoptosis in response to DNA damage; however, this resistance was abolished by coexpression of KLF2, which inhibits WEE1 transcription. Thus, the level of WEE1 is regulated by KLF2 and enhanced KLF2 expression sensitizes cells to DNA damage-induced apoptosis. © 2005 Nature Publishing Group. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectKLF2en_HK
dc.subjectTranscriptional regulationen_HK
dc.subjectWEE1en_HK
dc.titleTranscriptional repression of WEE1 by Kruppel-like factor 2 is involved in DNA damage-induced apoptosisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=24&issue=24&spage=3875&epage=3885&date=2005&atitle=Transcriptional+repression+of+WEE1+by+Kruppel-like+factor+2+is+involved+in+DNA+damage-induced+apoptosisen_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.onc.1208546en_HK
dc.identifier.scopuseid_2-s2.0-20544468698en_HK
dc.identifier.hkuros101900en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20544468698&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue24en_HK
dc.identifier.spage3875en_HK
dc.identifier.epage3885en_HK
dc.identifier.isiWOS:000229435300003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, F=7501309964en_HK
dc.identifier.scopusauthoridZhu, Y=7406071018en_HK
dc.identifier.scopusauthoridHuang, Y=55168797700en_HK
dc.identifier.scopusauthoridMcAvoy, S=9740784900en_HK
dc.identifier.scopusauthoridJohnson, WB=8593304500en_HK
dc.identifier.scopusauthoridCheung, TH=7103334169en_HK
dc.identifier.scopusauthoridChung, TKH=8866217800en_HK
dc.identifier.scopusauthoridLo, KWK=24302880900en_HK
dc.identifier.scopusauthoridYim, SF=7101624278en_HK
dc.identifier.scopusauthoridYu, MMY=8581464300en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridWong, YF=7403041448en_HK
dc.identifier.scopusauthoridSmith, DI=7410361498en_HK
dc.identifier.citeulike106674-

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