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Article: Identification and characterization of the hypoxia-responsive element in human stanniocalcin-1 gene

TitleIdentification and characterization of the hypoxia-responsive element in human stanniocalcin-1 gene
Authors
Issue Date2010
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mce
Citation
Molecular And Cellular Endocrinology, 2010, v. 314 n. 1, p. 118-127 How to Cite?
AbstractIn this study, we aimed to identify the hypoxia-inducible factor-1 (HIF-1) binding motif in human STC1 gene promoter and to characterize the associated gene transactivation mechanism. Using normoxic human nasopharyngeal cancer cells (CNE2), we manipulated the stability of HIF-1α protein by overexpressing HIF-1α or the silencing of prolyl hydroxylase-2 (PHD2), to illustrate HIF-1 activation of STC1 promoter-driven luciferase activity. Subsequently luciferase activities of the deletion and mutated STC1 promoter constructs were investigated in HIF-1 overexpressed cells. The data revealed the presence of an authentic HRE motif in STC1 gene. This result was further supported by the chromatin immunoprecipitation (ChIP) assay. Using a similar experimental treatment, however, had no significant effect on the expression level of STC1 mRNA and protein. Moreover the activation of STC1 expression can be restored by the silencing of "factor inhibiting HIF-1" (FIH-1) in either HIF-1 overexpressed or PHD2 silenced cells. The data implied that the HIF-1-mediated STC1 gene expression required the recruitment of p300. This presumption was confirmed by the use of p300 inhibitor, chetomin and HIF-1α/p300 re-ChIP assay. Collectively our data provide the first evidence to show that STC1 is a FIH-inhibited gene with a functional HRE motif located at the upstream region between -2322/-2335. The data support the need for further investigation to reveal if STC1 can be used as a novel tumor marker for HIF-1 induction and for the monitoring of anti-angiogenic therapy. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/183398
ISSN
2015 Impact Factor: 3.859
2015 SCImago Journal Rankings: 2.116
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, AYSen_US
dc.contributor.authorChing, LYen_US
dc.contributor.authorLai, KPen_US
dc.contributor.authorWong, CKCen_US
dc.date.accessioned2013-05-27T07:12:34Z-
dc.date.available2013-05-27T07:12:34Z-
dc.date.issued2010en_US
dc.identifier.citationMolecular And Cellular Endocrinology, 2010, v. 314 n. 1, p. 118-127en_US
dc.identifier.issn0303-7207en_US
dc.identifier.urihttp://hdl.handle.net/10722/183398-
dc.description.abstractIn this study, we aimed to identify the hypoxia-inducible factor-1 (HIF-1) binding motif in human STC1 gene promoter and to characterize the associated gene transactivation mechanism. Using normoxic human nasopharyngeal cancer cells (CNE2), we manipulated the stability of HIF-1α protein by overexpressing HIF-1α or the silencing of prolyl hydroxylase-2 (PHD2), to illustrate HIF-1 activation of STC1 promoter-driven luciferase activity. Subsequently luciferase activities of the deletion and mutated STC1 promoter constructs were investigated in HIF-1 overexpressed cells. The data revealed the presence of an authentic HRE motif in STC1 gene. This result was further supported by the chromatin immunoprecipitation (ChIP) assay. Using a similar experimental treatment, however, had no significant effect on the expression level of STC1 mRNA and protein. Moreover the activation of STC1 expression can be restored by the silencing of "factor inhibiting HIF-1" (FIH-1) in either HIF-1 overexpressed or PHD2 silenced cells. The data implied that the HIF-1-mediated STC1 gene expression required the recruitment of p300. This presumption was confirmed by the use of p300 inhibitor, chetomin and HIF-1α/p300 re-ChIP assay. Collectively our data provide the first evidence to show that STC1 is a FIH-inhibited gene with a functional HRE motif located at the upstream region between -2322/-2335. The data support the need for further investigation to reveal if STC1 can be used as a novel tumor marker for HIF-1 induction and for the monitoring of anti-angiogenic therapy. © 2009 Elsevier Ireland Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mceen_US
dc.relation.ispartofMolecular and Cellular Endocrinologyen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Hypoxia - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshGlycoproteins - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshHypoxia-Inducible Factor 1, Alpha Subunit - Genetics - Metabolismen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshRna, Small Interfering - Genetics - Metabolismen_US
dc.subject.meshResponse Elementsen_US
dc.subject.meshTranscriptional Activationen_US
dc.subject.meshP300-Cbp Transcription Factors - Metabolismen_US
dc.titleIdentification and characterization of the hypoxia-responsive element in human stanniocalcin-1 geneen_US
dc.typeArticleen_US
dc.identifier.emailLai, KP: ballllai@hotmail.comen_US
dc.identifier.authorityLai, KP=rp01753en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.mce.2009.07.007en_US
dc.identifier.pmid19628018-
dc.identifier.scopuseid_2-s2.0-70350182250en_US
dc.identifier.hkuros223779-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350182250&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume314en_US
dc.identifier.issue1en_US
dc.identifier.spage118en_US
dc.identifier.epage127en_US
dc.identifier.isiWOS:000272101700014-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridLaw, AYS=16175363700en_US
dc.identifier.scopusauthoridChing, LY=29367527200en_US
dc.identifier.scopusauthoridLai, KP=7402135707en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US

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