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Article: Regulation of angiogenesis by Id-1 through hypoxia-inducible factor-1α-mediated vascular endothelial growth factor up-regulation in hepatocellular carcinoma

TitleRegulation of angiogenesis by Id-1 through hypoxia-inducible factor-1α-mediated vascular endothelial growth factor up-regulation in hepatocellular carcinoma
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2006, v. 12 n. 23, p. 6910-6919 How to Cite?
AbstractPurpose: Metastasis is commonly associated with poor prognosis of hepatocellular carcinoma (HCC). Being an important angiogenic factor, vascular endothelial growth factor (VEGF) plays a central role in HCC growth and metastasis. Recently, Id-1 (inhibitor of differentiation/DNA synthesis) has been suggested to be a key factor in cancer progression but the molecular mechanism remains unknown. Experimental Design: We first showed that overexpression of Id-1 was correlated with HCC metastasis (P < 0.001) and its expression was significantly correlated with VEGF expression by tissue microarray. By ectopic transfection of Id-1 into HCC cells, Id-1 was able to induce VEGF secretion through activation of VEGF transcription. Results: Increased VEGF secretion in Id-1 transfectants induced morphologic change and proliferation of human umbilical vascular endothelial cell resulting in promotion of angiogenesis. Id-1 induced transcriptional activation of VEGF by stabilizing hypoxia-inducible factor-1α protein. Down-regulation of Id-1 by antisense approach led to suppression of hypoxia-inducible factor-1α-mediated VEGF production. In addition, Id-1 suppression resulted in retardation of cell invasion through down-regulation of VEGF. Conclusions: Id-1 is a novel angiogenic factor for HCC metastasis and down-regulation of Id-1 may be a novel target to inhibit HCC metastasis through suppression of angiogenesis. © 2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/148495
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, TKen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorYuen, APen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, XHen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorTang, ZYen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2012-05-29T06:13:18Z-
dc.date.available2012-05-29T06:13:18Z-
dc.date.issued2006en_HK
dc.identifier.citationClinical Cancer Research, 2006, v. 12 n. 23, p. 6910-6919en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148495-
dc.description.abstractPurpose: Metastasis is commonly associated with poor prognosis of hepatocellular carcinoma (HCC). Being an important angiogenic factor, vascular endothelial growth factor (VEGF) plays a central role in HCC growth and metastasis. Recently, Id-1 (inhibitor of differentiation/DNA synthesis) has been suggested to be a key factor in cancer progression but the molecular mechanism remains unknown. Experimental Design: We first showed that overexpression of Id-1 was correlated with HCC metastasis (P < 0.001) and its expression was significantly correlated with VEGF expression by tissue microarray. By ectopic transfection of Id-1 into HCC cells, Id-1 was able to induce VEGF secretion through activation of VEGF transcription. Results: Increased VEGF secretion in Id-1 transfectants induced morphologic change and proliferation of human umbilical vascular endothelial cell resulting in promotion of angiogenesis. Id-1 induced transcriptional activation of VEGF by stabilizing hypoxia-inducible factor-1α protein. Down-regulation of Id-1 by antisense approach led to suppression of hypoxia-inducible factor-1α-mediated VEGF production. In addition, Id-1 suppression resulted in retardation of cell invasion through down-regulation of VEGF. Conclusions: Id-1 is a novel angiogenic factor for HCC metastasis and down-regulation of Id-1 may be a novel target to inhibit HCC metastasis through suppression of angiogenesis. © 2006 American Association for Cancer Research.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshCarcinoma, Hepatocellular - Drug Therapy - Physiopathology - Secondaryen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshDown-Regulation - Drug Effectsen_US
dc.subject.meshEndothelial Cells - Drug Effectsen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshHumansen_US
dc.subject.meshHypoxia-Inducible Factor 1, Alpha Subunit - Metabolismen_US
dc.subject.meshInhibitor Of Differentiation Protein 1 - Antagonists & Inhibitors - Genetics - Metabolismen_US
dc.subject.meshLiver Neoplasms - Drug Therapy - Physiopathology - Secondaryen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNeovascularization, Pathologic - Metabolismen_US
dc.subject.meshOligodeoxyribonucleotides, Antisense - Pharmacology - Therapeutic Useen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshStructure-Activity Relationshipen_US
dc.subject.meshTissue Array Analysisen_US
dc.subject.meshTransplantation, Heterologousen_US
dc.subject.meshVascular Endothelial Growth Factor A - Genetics - Metabolism - Secretionen_US
dc.subject.meshXenograft Model Antitumor Assaysen_US
dc.titleRegulation of angiogenesis by Id-1 through hypoxia-inducible factor-1α-mediated vascular endothelial growth factor up-regulation in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, TK:tkwlee@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP:poontp@hkucc.hku.hken_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.emailMan, K:kwanman@hkucc.hku.hken_HK
dc.identifier.emailFan, ST:stfan@hku.hken_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1158/1078-0432.CCR-06-0489en_HK
dc.identifier.pmid17145808-
dc.identifier.scopuseid_2-s2.0-33845760019en_HK
dc.identifier.hkuros137542-
dc.identifier.hkuros125160-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845760019&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue23en_HK
dc.identifier.spage6910en_HK
dc.identifier.epage6919en_HK
dc.identifier.isiWOS:000242691000007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridYuen, AP=7006290111en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWang, XH=7501854829en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridTang, ZY=15752346400en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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