File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The gold (III) porphyrin complex, gold-2a, suppresses WNT1 expression in breast cancer cells by enhancing the promoter association of YY1

TitleThe gold (III) porphyrin complex, gold-2a, suppresses WNT1 expression in breast cancer cells by enhancing the promoter association of YY1
Authors
KeywordsPorphyrin derivative
Transcription factor YY1
Antineoplastic activity
Bioaccumulation
Breast cancer
Issue Date2011
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.org
Citation
American Journal of Translational Research, 2011, v. 3 n. 5, p. 479-491 How to Cite?
AbstractThe gold (III) porphyrin complex, gold-2a, elicits anti-tumor activity by targeting the Wnt/beta-catenin signaling pathway [Chow KH et al, Cancer Research 2010;70(1):329-37]. Here, the molecular mechanisms underlying the inhibitory effects of this compound on WNT1 gene expression were elucidated further. A response element to gold-2a was identified located within the -1290 to -1112 nt region of the WNT1 promoter, containing a binding site for the transcription regulator Yin Yang 1 (YY1). Gold-2a promoted the association of YY1 and suppressor of zeste 12 (Suz12; a component of the polycomb repressor complex 2) with the WNT1 promoter. Under normal culture conditions, the intracellular translocalization of YY1 was synchronized with cell cycle progression and WNT1 expression. Gold-2a promoted the nuclear accumulation and abolished the nuclear exportation of YY1, resulting in a persistent inhibition of WNT1 expression and a cell cycle arrest at G1/S phase. A dimorphic role of YY1 in regulating cell proliferation and division was revealed. Thus, the present study extends the understanding of the anti-tumor mechanism of gold-2a to the epigenetic level, which involves the modulation of the dynamic interactions between YY1 and a specific region of the WNT1 promoter.
Persistent Identifierhttp://hdl.handle.net/10722/163410
ISSN
2015 Impact Factor: 3.146
2015 SCImago Journal Rankings: 1.442
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChow, KHMen_HK
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorSun, RWYen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorChen, Jen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2012-09-05T05:31:02Z-
dc.date.available2012-09-05T05:31:02Z-
dc.date.issued2011en_HK
dc.identifier.citationAmerican Journal of Translational Research, 2011, v. 3 n. 5, p. 479-491en_HK
dc.identifier.issn1943-8141en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163410-
dc.description.abstractThe gold (III) porphyrin complex, gold-2a, elicits anti-tumor activity by targeting the Wnt/beta-catenin signaling pathway [Chow KH et al, Cancer Research 2010;70(1):329-37]. Here, the molecular mechanisms underlying the inhibitory effects of this compound on WNT1 gene expression were elucidated further. A response element to gold-2a was identified located within the -1290 to -1112 nt region of the WNT1 promoter, containing a binding site for the transcription regulator Yin Yang 1 (YY1). Gold-2a promoted the association of YY1 and suppressor of zeste 12 (Suz12; a component of the polycomb repressor complex 2) with the WNT1 promoter. Under normal culture conditions, the intracellular translocalization of YY1 was synchronized with cell cycle progression and WNT1 expression. Gold-2a promoted the nuclear accumulation and abolished the nuclear exportation of YY1, resulting in a persistent inhibition of WNT1 expression and a cell cycle arrest at G1/S phase. A dimorphic role of YY1 in regulating cell proliferation and division was revealed. Thus, the present study extends the understanding of the anti-tumor mechanism of gold-2a to the epigenetic level, which involves the modulation of the dynamic interactions between YY1 and a specific region of the WNT1 promoter.en_HK
dc.languageengen_US
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.orgen_HK
dc.relation.ispartofAmerican Journal of Translational Researchen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectPorphyrin derivativeen_HK
dc.subjectTranscription factor YY1en_HK
dc.subjectAntineoplastic activityen_HK
dc.subjectBioaccumulationen_HK
dc.subjectBreast canceren_HK
dc.titleThe gold (III) porphyrin complex, gold-2a, suppresses WNT1 expression in breast cancer cells by enhancing the promoter association of YY1en_HK
dc.typeArticleen_HK
dc.identifier.emailLiu, J: jingliue@hku.hken_HK
dc.identifier.emailSun, RWY: rwysun@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailChe, CM: cmche@hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authoritySun, RWY=rp00781en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.pmid22046489-
dc.identifier.pmcidPMC3204891-
dc.identifier.scopuseid_2-s2.0-80054744541en_HK
dc.identifier.hkuros204853-
dc.identifier.hkuros221741-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054744541&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue5en_HK
dc.identifier.spage479en_HK
dc.identifier.epage491en_HK
dc.identifier.isiWOS:000208694900007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridChe, CM=7102442791en_HK
dc.identifier.scopusauthoridChen, J=54381352900en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridSun, RWY=26325835800en_HK
dc.identifier.scopusauthoridLiu, J=36066808300en_HK
dc.identifier.scopusauthoridChow, KHM=26430472800en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats