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Article: Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway

TitleId-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway
Authors
Issue Date2002
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2002, v. 23 n. 5, p. 721-725 How to Cite?
AbstractIt has been suggested that the helix-loop-helix protein Id-1 plays an important role in tumourigenesis in certain types of human cancer. Previously, we reported that Id-1 was up-regulated during sex hormone-induced prostate carcinogenesis in a Noble rat model (Ouyang et al. (2001) Carcinogenesis, 22, 965-973). In the present study, we investigated the direct effect of Id-1 expression on human prostate cancer cell proliferation by transfecting an Id-1 expression vector into a prostate cancer cell line LNCaP. Ten stable transfectant clones were isolated and the ectopic Id-1 expression resulted in both increased DNA synthesis rate and the percentage of S phase cells. To study the possible mechanisms involved in the Id-1 induced prostate cancer cell growth, we examined the expression of several factors responsible for G1 to S phase progression. We found that Id-1 expression induced phosphorylation of RB and down-regulation of p16INK4a but not p21Waf1 or p27Kip1. Our results indicate that the Id-1 induced inactivation of p16INK4a/pRB pathway may be responsible for the increased cell proliferation in prostate cancer cells. Given the fact that both Id-1 over-expression and inactivation of p16INK4a/ pRB are common events in prostate cancer, our results provide a possible mechanism on the molecular basis of prostate carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/149607
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorOuyang, XSen_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorWong, HLen_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorWong, YCen_US
dc.date.accessioned2012-06-26T05:55:54Z-
dc.date.available2012-06-26T05:55:54Z-
dc.date.issued2002en_US
dc.identifier.citationCarcinogenesis, 2002, v. 23 n. 5, p. 721-725en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10722/149607-
dc.description.abstractIt has been suggested that the helix-loop-helix protein Id-1 plays an important role in tumourigenesis in certain types of human cancer. Previously, we reported that Id-1 was up-regulated during sex hormone-induced prostate carcinogenesis in a Noble rat model (Ouyang et al. (2001) Carcinogenesis, 22, 965-973). In the present study, we investigated the direct effect of Id-1 expression on human prostate cancer cell proliferation by transfecting an Id-1 expression vector into a prostate cancer cell line LNCaP. Ten stable transfectant clones were isolated and the ectopic Id-1 expression resulted in both increased DNA synthesis rate and the percentage of S phase cells. To study the possible mechanisms involved in the Id-1 induced prostate cancer cell growth, we examined the expression of several factors responsible for G1 to S phase progression. We found that Id-1 expression induced phosphorylation of RB and down-regulation of p16INK4a but not p21Waf1 or p27Kip1. Our results indicate that the Id-1 induced inactivation of p16INK4a/pRB pathway may be responsible for the increased cell proliferation in prostate cancer cells. Given the fact that both Id-1 over-expression and inactivation of p16INK4a/ pRB are common events in prostate cancer, our results provide a possible mechanism on the molecular basis of prostate carcinogenesis.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.subject.meshBlooden_US
dc.subject.meshCell Cycle - Physiologyen_US
dc.subject.meshCell Division - Physiologyen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P16 - Antagonists & Inhibitorsen_US
dc.subject.meshDna Replication - Physiologyen_US
dc.subject.meshDna-Binding Proteins - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1en_US
dc.subject.meshMaleen_US
dc.subject.meshProstatic Neoplasms - Pathologyen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshRetinoblastoma Protein - Antagonists & Inhibitorsen_US
dc.subject.meshTranscription Factors - Physiologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleId-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid12016143-
dc.identifier.scopuseid_2-s2.0-0036258713en_US
dc.identifier.hkuros66105-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036258713&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume23en_US
dc.identifier.issue5en_US
dc.identifier.spage721en_US
dc.identifier.epage725en_US
dc.identifier.isiWOS:000175879000006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridOuyang, XS=8711278300en_US
dc.identifier.scopusauthoridWang, X=7501854829en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWong, HL=7402862563en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US

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