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Article: Suppression of hypoxia inducible factor-1α (HIF-1α) by YC-1 is dependent on murine double minute 2 (Mdm2)

TitleSuppression of hypoxia inducible factor-1α (HIF-1α) by YC-1 is dependent on murine double minute 2 (Mdm2)
Authors
KeywordsHepatocellular carcinoma
Hypoxia inducible factor-1α
Murine double minute 2
YC-1
Issue Date2006
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2006, v. 348 n. 4, p. 1443-1448 How to Cite?
AbstractInhibition of HIF-1α activity provides an important strategy for the treatment of cancer. Recently, 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) has been identified as an anti-HIF-1α drug in cancer therapy with unclear molecular mechanism. In the present study, we aimed to investigate the effect and mechanism of YC-1 on HIF-1α in a hepatocellular carcinoma cell line under hypoxic condition, which was generated by incubating cells with 0.1% O2. The phenotypic and molecular changes of cells were determined by cell proliferation assay, apoptosis assay, luciferase promoter assay, and Western blot analysis. YC-1 arrested tumor cell growth in a dose-dependent manner, whereas it did not induce cell apoptosis. Hypoxia-induced upregulation of HIF-1α was suppressed by YC-1 administration. YC-1 inhibited HIF-1α protein synthesis under normoxia and affected protein stability under hypoxia. YC-1 suppressed the expression of total and phosphorylated forms of murine double minute 2 (Mdm2), whereas this inhibitory effect was blocked by overexpression of Mdm2. In conclusion, YC-1 suppressed both protein synthesis and stability of HIF-1α in HCC cells, and its inhibitory effects on HIF-1α were dependent on Mdm2. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/54335
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLau, CKen_HK
dc.contributor.authorYang, ZFen_HK
dc.contributor.authorLam, CTen_HK
dc.contributor.authorTam, KHen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2009-04-03T07:43:40Z-
dc.date.available2009-04-03T07:43:40Z-
dc.date.issued2006en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2006, v. 348 n. 4, p. 1443-1448en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/54335-
dc.description.abstractInhibition of HIF-1α activity provides an important strategy for the treatment of cancer. Recently, 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) has been identified as an anti-HIF-1α drug in cancer therapy with unclear molecular mechanism. In the present study, we aimed to investigate the effect and mechanism of YC-1 on HIF-1α in a hepatocellular carcinoma cell line under hypoxic condition, which was generated by incubating cells with 0.1% O2. The phenotypic and molecular changes of cells were determined by cell proliferation assay, apoptosis assay, luciferase promoter assay, and Western blot analysis. YC-1 arrested tumor cell growth in a dose-dependent manner, whereas it did not induce cell apoptosis. Hypoxia-induced upregulation of HIF-1α was suppressed by YC-1 administration. YC-1 inhibited HIF-1α protein synthesis under normoxia and affected protein stability under hypoxia. YC-1 suppressed the expression of total and phosphorylated forms of murine double minute 2 (Mdm2), whereas this inhibitory effect was blocked by overexpression of Mdm2. In conclusion, YC-1 suppressed both protein synthesis and stability of HIF-1α in HCC cells, and its inhibitory effects on HIF-1α were dependent on Mdm2. © 2006 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectHepatocellular carcinomaen_HK
dc.subjectHypoxia inducible factor-1αen_HK
dc.subjectMurine double minute 2en_HK
dc.subjectYC-1en_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathologyen_HK
dc.subject.meshCell Hypoxiaen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshDown-Regulationen_HK
dc.titleSuppression of hypoxia inducible factor-1α (HIF-1α) by YC-1 is dependent on murine double minute 2 (Mdm2)en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=348&issue=4&spage=1443&epage=1448&date=2006&atitle=Suppression+of+hypoxia+inducible+factor-1a+(HIF-1a)+by+YC-1+is+dependent+on+murine+double+minute+2+(Mdm2)en_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1016/j.bbrc.2006.08.015en_HK
dc.identifier.pmid16919599-
dc.identifier.scopuseid_2-s2.0-33747888997en_HK
dc.identifier.hkuros120196-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33747888997&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume348en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1443en_HK
dc.identifier.epage1448en_HK
dc.identifier.isiWOS:000240425600031-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLau, CK=7401968442en_HK
dc.identifier.scopusauthoridYang, ZF=14018809600en_HK
dc.identifier.scopusauthoridLam, CT=7402989860en_HK
dc.identifier.scopusauthoridTam, KH=7201692833en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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