File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Prostate cancer: The Id1 story

TitleProstate cancer: The Id1 story
Authors
KeywordsAndrogen independent prostate cancer
Id1 gene
Issue Date2004
PublisherNihon Soshiki Saibo Kagakukai. The Journal's web site is located at http://www.jstage.jst.go.jp/browse/ahc/_vols/-char/en
Citation
Acta Histochemica Et Cytochemica, 2004, v. 37 n. 6, p. 331-337 How to Cite?
AbstractId (inhibitor of differentiation or DNA binding) gene encodes a helix-loop helix protein which dimerizes and blocks the basic HLH protein from binding DNA. It expresses mainly in actively dividing cells and was first reported to be involved in hormone-induced prostate cancer in the Noble rat model. It was subsequently confirmed also in human prostate cancer. Through functional studies under in vitro system, they have further demonstrated the role of Id1 in prostate cancer progression. They have shown that Id1 transfection stimulated prostate cancer cell proliferation through downregulation of p16/Rb, while inducing activation of MAPK and NFκB pathways. Activation of the latter pathways by ectopic transfection of Id1 to LNCaP cells, an androgen dependent line, also resulted in reduced sensitivity of prostate cancer cells to androgen on the one hand and upregulating the expression of EGFR and PSA on the other hand, which are both hallmarks of androgen independent prostate cancer. This review shows the crucial role played by Id1 in the conversion of prostate cancer from androgen dependent to androgen independent stage.
Persistent Identifierhttp://hdl.handle.net/10722/67546
ISSN
2015 Impact Factor: 0.912
2015 SCImago Journal Rankings: 0.589
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, XHen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorOuyang, XSen_HK
dc.contributor.authorChan, FLen_HK
dc.date.accessioned2010-09-06T05:56:06Z-
dc.date.available2010-09-06T05:56:06Z-
dc.date.issued2004en_HK
dc.identifier.citationActa Histochemica Et Cytochemica, 2004, v. 37 n. 6, p. 331-337en_HK
dc.identifier.issn0044-5991en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67546-
dc.description.abstractId (inhibitor of differentiation or DNA binding) gene encodes a helix-loop helix protein which dimerizes and blocks the basic HLH protein from binding DNA. It expresses mainly in actively dividing cells and was first reported to be involved in hormone-induced prostate cancer in the Noble rat model. It was subsequently confirmed also in human prostate cancer. Through functional studies under in vitro system, they have further demonstrated the role of Id1 in prostate cancer progression. They have shown that Id1 transfection stimulated prostate cancer cell proliferation through downregulation of p16/Rb, while inducing activation of MAPK and NFκB pathways. Activation of the latter pathways by ectopic transfection of Id1 to LNCaP cells, an androgen dependent line, also resulted in reduced sensitivity of prostate cancer cells to androgen on the one hand and upregulating the expression of EGFR and PSA on the other hand, which are both hallmarks of androgen independent prostate cancer. This review shows the crucial role played by Id1 in the conversion of prostate cancer from androgen dependent to androgen independent stage.en_HK
dc.languageengen_HK
dc.publisherNihon Soshiki Saibo Kagakukai. The Journal's web site is located at http://www.jstage.jst.go.jp/browse/ahc/_vols/-char/enen_HK
dc.relation.ispartofActa Histochemica et Cytochemicaen_HK
dc.subjectAndrogen independent prostate canceren_HK
dc.subjectId1 geneen_HK
dc.titleProstate cancer: The Id1 storyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1936-0851&volume=37&issue=6&spage=331&epage=337&date=2005&atitle=Prostate+Cancer:+The+Id1+Storyen_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1267/ahc.37.331en_HK
dc.identifier.scopuseid_2-s2.0-15744403157en_HK
dc.identifier.hkuros97665en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-15744403157&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue6en_HK
dc.identifier.spage331en_HK
dc.identifier.epage337en_HK
dc.identifier.isiWOS:000227569500001-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, XH=7501854829en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridOuyang, XS=8711278300en_HK
dc.identifier.scopusauthoridChan, FL=7202586505en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats