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- Publisher Website: 10.1093/carcin/23.5.721
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- PMID: 12016143
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Article: Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway
Title | Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway |
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Authors | |
Issue Date | 2002 |
Publisher | Oxford 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? |
Abstract | It 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 Identifier | http://hdl.handle.net/10722/149607 |
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.074 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ouyang, XS | en_US |
dc.contributor.author | Wang, X | en_US |
dc.contributor.author | Ling, MT | en_US |
dc.contributor.author | Wong, HL | en_US |
dc.contributor.author | Tsao, SW | en_US |
dc.contributor.author | Wong, YC | en_US |
dc.date.accessioned | 2012-06-26T05:55:54Z | - |
dc.date.available | 2012-06-26T05:55:54Z | - |
dc.date.issued | 2002 | en_US |
dc.identifier.citation | Carcinogenesis, 2002, v. 23 n. 5, p. 721-725 | en_US |
dc.identifier.issn | 0143-3334 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/149607 | - |
dc.description.abstract | It 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.language | eng | en_US |
dc.publisher | Oxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/ | en_US |
dc.relation.ispartof | Carcinogenesis | en_US |
dc.subject.mesh | Blood | en_US |
dc.subject.mesh | Cell Cycle - Physiology | en_US |
dc.subject.mesh | Cell Division - Physiology | en_US |
dc.subject.mesh | Cyclin-Dependent Kinase Inhibitor P16 - Antagonists & Inhibitors | en_US |
dc.subject.mesh | Dna Replication - Physiology | en_US |
dc.subject.mesh | Dna-Binding Proteins - Physiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Inhibitor Of Differentiation Protein 1 | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Prostatic Neoplasms - Pathology | en_US |
dc.subject.mesh | Repressor Proteins | en_US |
dc.subject.mesh | Retinoblastoma Protein - Antagonists & Inhibitors | en_US |
dc.subject.mesh | Transcription Factors - Physiology | en_US |
dc.subject.mesh | Tumor Cells, Cultured | en_US |
dc.title | Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway | en_US |
dc.type | Article | en_US |
dc.identifier.email | Ling, MT:patling@hkucc.hku.hk | en_US |
dc.identifier.email | Tsao, SW:gswtsao@hkucc.hku.hk | en_US |
dc.identifier.email | Wong, YC:ycwong@hkucc.hku.hk | en_US |
dc.identifier.authority | Ling, MT=rp00449 | en_US |
dc.identifier.authority | Tsao, SW=rp00399 | en_US |
dc.identifier.authority | Wong, YC=rp00316 | en_US |
dc.description.nature | link_to_OA_fulltext | en_US |
dc.identifier.doi | 10.1093/carcin/23.5.721 | - |
dc.identifier.pmid | 12016143 | - |
dc.identifier.scopus | eid_2-s2.0-0036258713 | en_US |
dc.identifier.hkuros | 66105 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0036258713&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 23 | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.spage | 721 | en_US |
dc.identifier.epage | 725 | en_US |
dc.identifier.isi | WOS:000175879000006 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Ouyang, XS=8711278300 | en_US |
dc.identifier.scopusauthorid | Wang, X=7501854829 | en_US |
dc.identifier.scopusauthorid | Ling, MT=7102229780 | en_US |
dc.identifier.scopusauthorid | Wong, HL=7402862563 | en_US |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_US |
dc.identifier.scopusauthorid | Wong, YC=7403041798 | en_US |
dc.identifier.issnl | 0143-3334 | - |