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Article: Overexpression of Id-1 in prostate cancer cells promotes angiogenesis through the activation of vascular endothelial growth factor (VEGF)

TitleOverexpression of Id-1 in prostate cancer cells promotes angiogenesis through the activation of vascular endothelial growth factor (VEGF)
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2005, v. 26 n. 10, p. 1668-1676 How to Cite?
AbstractAndrogen-independent metastatic prostate cancer is the main cause of cancer related death in men. One of the reasons for this is the lack of understanding of the molecular mechanisms leading to the metastatic progression of prostate cancer. In this study, we have demonstrated that overexpression of Id-1 (inhibitor of differentiation/DNA synthesis), a member of the helix-loop-helix family proteins, is a key factor in promoting angiogenesis through activation of the vascular endothelial growth factor (VEGF) in prostate cancer cells. Using prostate cancer cells ectopically transfected with the Id-1 gene, we found that upregulation of Id-1 induced VEGF secretion through activation of the VEGF gene transcription. Downregulation of Id-1, however, led to the suppression of VEGF secretion and its gene promoter activity. The association between Id-1 and VEGF was also confirmed on human xenografts by immunohistochemical staining. In addition, the growth medium generated by the Id-1 expressing cells was able to promote morphological changes as well as capillary tube formation in human umbilical vein endothelial cells (HUVECs) at similar degrees to the recombinant human VEGF. Furthermore, inhibition of VEGF function by the treatment with an Flk-1 inhibitor, SU1498, or with the VEGF neutralizing antibody resulted in the reverse of the angiogenic effect on HUVECs. Our results suggest that overexpression of Id-1 in prostate cancer cells may provide an autocrine signal to promote angiogenesis through the activation of VEGF. Since increased Id-1 has been reported in many types of advanced human cancers, our results indicate that downregulation of Id-1 may be a novel target to inhibit the growth of metastatic cancers through the suppression of angiogenesis. © Oxford University Press 2005; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149645
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_US
dc.contributor.authorLau, TCMen_US
dc.contributor.authorZhou, Cen_US
dc.contributor.authorChua, CWen_US
dc.contributor.authorKwok, WKen_US
dc.contributor.authorWang, Qen_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorWong, YCen_US
dc.date.accessioned2012-06-26T05:56:27Z-
dc.date.available2012-06-26T05:56:27Z-
dc.date.issued2005en_US
dc.identifier.citationCarcinogenesis, 2005, v. 26 n. 10, p. 1668-1676en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10722/149645-
dc.description.abstractAndrogen-independent metastatic prostate cancer is the main cause of cancer related death in men. One of the reasons for this is the lack of understanding of the molecular mechanisms leading to the metastatic progression of prostate cancer. In this study, we have demonstrated that overexpression of Id-1 (inhibitor of differentiation/DNA synthesis), a member of the helix-loop-helix family proteins, is a key factor in promoting angiogenesis through activation of the vascular endothelial growth factor (VEGF) in prostate cancer cells. Using prostate cancer cells ectopically transfected with the Id-1 gene, we found that upregulation of Id-1 induced VEGF secretion through activation of the VEGF gene transcription. Downregulation of Id-1, however, led to the suppression of VEGF secretion and its gene promoter activity. The association between Id-1 and VEGF was also confirmed on human xenografts by immunohistochemical staining. In addition, the growth medium generated by the Id-1 expressing cells was able to promote morphological changes as well as capillary tube formation in human umbilical vein endothelial cells (HUVECs) at similar degrees to the recombinant human VEGF. Furthermore, inhibition of VEGF function by the treatment with an Flk-1 inhibitor, SU1498, or with the VEGF neutralizing antibody resulted in the reverse of the angiogenic effect on HUVECs. Our results suggest that overexpression of Id-1 in prostate cancer cells may provide an autocrine signal to promote angiogenesis through the activation of VEGF. Since increased Id-1 has been reported in many types of advanced human cancers, our results indicate that downregulation of Id-1 may be a novel target to inhibit the growth of metastatic cancers through the suppression of angiogenesis. © Oxford University Press 2005; all rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_US
dc.relation.ispartofCarcinogenesisen_US
dc.rightsCarcinogenesis. Copyright © Oxford University Press.-
dc.subject.meshAdenocarcinoma - Blood Supply - Genetics - Pathologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1en_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshNeovascularization, Pathologic - Geneticsen_US
dc.subject.meshProstatic Neoplasms - Blood Supply - Genetics - Pathologyen_US
dc.subject.meshRepressor Proteins - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTranscription Factors - Geneticsen_US
dc.subject.meshTransfectionen_US
dc.subject.meshUmbilical Veinsen_US
dc.subject.meshVascular Endothelial Growth Factor A - Geneticsen_US
dc.titleOverexpression of Id-1 in prostate cancer cells promotes angiogenesis through the activation of vascular endothelial growth factor (VEGF)en_US
dc.typeArticleen_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/carcin/bgi128en_US
dc.identifier.pmid15905202-
dc.identifier.scopuseid_2-s2.0-27144471048en_US
dc.identifier.hkuros108877-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27144471048&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume26en_US
dc.identifier.issue10en_US
dc.identifier.spage1668en_US
dc.identifier.epage1676en_US
dc.identifier.isiWOS:000232103100003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridLau, TCM=17341008600en_US
dc.identifier.scopusauthoridZhou, C=8643084400en_US
dc.identifier.scopusauthoridChua, CW=9437494600en_US
dc.identifier.scopusauthoridKwok, WK=8578541800en_US
dc.identifier.scopusauthoridWang, Q=7406910452en_US
dc.identifier.scopusauthoridWang, X=7501854829en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.citeulike328901-

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