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Article: CDK5RAP3 is a novel repressor of p14ARF in hepatocellular carcinoma cells
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TitleCDK5RAP3 is a novel repressor of p14ARF in hepatocellular carcinoma cells
 
AuthorsMak, GWY1
Lai, WL1
Zhou, Y1
Li, M3
Ng, IOL1 2
Ching, YP1 2
 
Issue Date2012
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPLoS One, 2012, v. 7 n. 7, article no. e42210 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0042210
 
AbstractCDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a novel activator of PAK4 and processes important pro-metastatic function in hepatocarcinogenesis. However, it remains unclear if there are other mechanisms by which CDK5RAP3 promotes HCC metastasis. Here, we showed that in CDK5RAP3 stable knockdown SMMC-7721 HCC cells, p14(ARF) tumor suppressor was upregulated at protein and mRNA levels, and ectopic expression of CDK5RAP3 was found to repress the transcription of p14(ARF). Using chromatin immunoprecipitation assay, we demonstrated that CDK5RAP3 bound to p14(ARF) promoter in vivo. Furthermore, knockdown of p14(ARF) in CDK5RAP3 stable knockdown HCC cells reversed the suppression of HCC cell invasiveness mediated by knockdown of CDK5RAP3. Taken together, our findings provide the new evidence that overexpression of CDK5RAP3 promotes HCC metastasis via downregulation of p14(ARF).
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0042210
 
PubMed Central IDPMC3409131
 
DC FieldValue
dc.contributor.authorMak, GWY
 
dc.contributor.authorLai, WL
 
dc.contributor.authorZhou, Y
 
dc.contributor.authorLi, M
 
dc.contributor.authorNg, IOL
 
dc.contributor.authorChing, YP
 
dc.date.accessioned2012-08-16T05:47:31Z
 
dc.date.available2012-08-16T05:47:31Z
 
dc.date.issued2012
 
dc.description.abstractCDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a novel activator of PAK4 and processes important pro-metastatic function in hepatocarcinogenesis. However, it remains unclear if there are other mechanisms by which CDK5RAP3 promotes HCC metastasis. Here, we showed that in CDK5RAP3 stable knockdown SMMC-7721 HCC cells, p14(ARF) tumor suppressor was upregulated at protein and mRNA levels, and ectopic expression of CDK5RAP3 was found to repress the transcription of p14(ARF). Using chromatin immunoprecipitation assay, we demonstrated that CDK5RAP3 bound to p14(ARF) promoter in vivo. Furthermore, knockdown of p14(ARF) in CDK5RAP3 stable knockdown HCC cells reversed the suppression of HCC cell invasiveness mediated by knockdown of CDK5RAP3. Taken together, our findings provide the new evidence that overexpression of CDK5RAP3 promotes HCC metastasis via downregulation of p14(ARF).
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPLoS One, 2012, v. 7 n. 7, article no. e42210 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0042210
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0042210
 
dc.identifier.hkuros202170
 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue7, article no. e42210
 
dc.identifier.pmcidPMC3409131
 
dc.identifier.pmid22860085
 
dc.identifier.scopuseid_2-s2.0-84864454197
 
dc.identifier.urihttp://hdl.handle.net/10722/159261
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS One
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.titleCDK5RAP3 is a novel repressor of p14ARF in hepatocellular carcinoma cells
 
dc.typeArticle
 
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<contributor.author>Lai, WL</contributor.author>
<contributor.author>Zhou, Y</contributor.author>
<contributor.author>Li, M</contributor.author>
<contributor.author>Ng, IOL</contributor.author>
<contributor.author>Ching, YP</contributor.author>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. The University of Hong Kong
  3. Sun Yat-Sen University