File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The multiple roles of Id-1 in cancer progression

TitleThe multiple roles of Id-1 in cancer progression
Authors
Issue Date2006
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DIF
Citation
Differentiation, 2006, v. 74 n. 9-10, p. 481-487 How to Cite?
AbstractId-1 (Inhibitor of differentiation/DNA binding) is a member of the helix-loop-helix protein family expressed in actively proliferating cells. It regulates gene transcription by heterodimerization with the basic helix-loop-helix transcription factors and therefore inhibits them from DNA binding and transactivation of their target genes. Early studies showed that Id-1 functions mainly as a regulator in cellular differentiation of the muscle cells. The oncogenic role of Id-1 was revealed recently by the finding that Id-1 expression was able to induce cancer cell growth and promote cell survival. In addition, Id-1 protein was frequently overexpressed in over 20 types of cancer, supporting its role in the tumorigenesis of a wide range of tissues. However, the fact that Id-1 was able to activate multiple pathways involved in tumor progression suggests that Id-1 may in addition function in promotion of tumor development. For example, overexpression of Id-1 was found to induce expression of MT1-MMP protein, leading to invasion of breast cancer cells. A close association between Id-1 expression and angiogenesis has also been demonstrated recently in both normal and cancer cells. Accordingly, in prostate cancer cells, expression of Id-1 was able to activate EGF-R and nuclear factor-κB activities and resulted in progression to androgen independence. In addition, in both nasopharyngeal carcinoma and prostate cancer cells, Id-1 expression was found to protect the cells from chemotherapeutic drug-induced apoptosis through regulation of the Raf-1/MAPK and JNK pathways. This review will discuss recent evidence supporting the role of Id-1 in tumor progression and the mechanisms involved. © 2006, International Society of Differentiation.
Persistent Identifierhttp://hdl.handle.net/10722/67711
ISSN
2015 Impact Factor: 2.461
2015 SCImago Journal Rankings: 1.747
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:57:34Z-
dc.date.available2010-09-06T05:57:34Z-
dc.date.issued2006en_HK
dc.identifier.citationDifferentiation, 2006, v. 74 n. 9-10, p. 481-487en_HK
dc.identifier.issn0301-4681en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67711-
dc.description.abstractId-1 (Inhibitor of differentiation/DNA binding) is a member of the helix-loop-helix protein family expressed in actively proliferating cells. It regulates gene transcription by heterodimerization with the basic helix-loop-helix transcription factors and therefore inhibits them from DNA binding and transactivation of their target genes. Early studies showed that Id-1 functions mainly as a regulator in cellular differentiation of the muscle cells. The oncogenic role of Id-1 was revealed recently by the finding that Id-1 expression was able to induce cancer cell growth and promote cell survival. In addition, Id-1 protein was frequently overexpressed in over 20 types of cancer, supporting its role in the tumorigenesis of a wide range of tissues. However, the fact that Id-1 was able to activate multiple pathways involved in tumor progression suggests that Id-1 may in addition function in promotion of tumor development. For example, overexpression of Id-1 was found to induce expression of MT1-MMP protein, leading to invasion of breast cancer cells. A close association between Id-1 expression and angiogenesis has also been demonstrated recently in both normal and cancer cells. Accordingly, in prostate cancer cells, expression of Id-1 was able to activate EGF-R and nuclear factor-κB activities and resulted in progression to androgen independence. In addition, in both nasopharyngeal carcinoma and prostate cancer cells, Id-1 expression was found to protect the cells from chemotherapeutic drug-induced apoptosis through regulation of the Raf-1/MAPK and JNK pathways. This review will discuss recent evidence supporting the role of Id-1 in tumor progression and the mechanisms involved. © 2006, International Society of Differentiation.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DIFen_HK
dc.relation.ispartofDifferentiationen_HK
dc.rightsDifferentiation. Copyright © Elsevier Ltd.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshDrug Resistance, Neoplasmen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - metabolism - physiologyen_HK
dc.subject.meshModels, Biologicalen_HK
dc.subject.meshNeoplasms - etiology - metabolism - therapyen_HK
dc.titleThe multiple roles of Id-1 in cancer progressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0301-4681&volume=74&spage=481&epage=487&date=2006&atitle=The+multiple+roles+of+Id-1+in+cancer+progressionen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1432-0436.2006.00083.xen_HK
dc.identifier.pmid17177845en_HK
dc.identifier.scopuseid_2-s2.0-33845529632en_HK
dc.identifier.hkuros127169en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845529632&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume74en_HK
dc.identifier.issue9-10en_HK
dc.identifier.spage481en_HK
dc.identifier.epage487en_HK
dc.identifier.isiWOS:000242657200001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridZhang, X=8578540900en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.citeulike966401-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats