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Article: Identification of carboxypeptidase of glutamate like-B as a candidate suppressor in cell growth and metastasis in human hepatocellular carcinoma
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TitleIdentification of carboxypeptidase of glutamate like-B as a candidate suppressor in cell growth and metastasis in human hepatocellular carcinoma
 
AuthorsZhang, P2
Chan, DW1
Yi, YZ2
Jin, JL2
Ng, IOL1
Wan, D2
Gu, J2
 
Issue Date2006
 
PublisherAmerican Association for Cancer Research.
 
CitationClinical Cancer Research, 2006, v. 12 n. 22, p. 6617-6625 [How to Cite?]
DOI: http://dx.doi.org/10.1158/1078-0432.CCR-06-1307
 
AbstractPurpose: We have previously done large-scale cDNA transfection screening on human hepatocellular carcinoma (HCC) cells and have identified 3,806 cDNA genes that possess the ability of either stimulating or inhibiting cell growth. In this study, we characterized one of these growth suppressor genes, carboxypeptidase of glutamate like-B (CPGL-B), in HCC. Experimental Design: Semiquantitative reverse-transcription PCR was used to examine the expression levels of CPGL-B. The cellular localization and functions of CPGL-B were investigated by enforced expression of CPGL-B in HCC cells. Results: From our previous cDNA transfection screening, we identified a gene named CPGL and its isoform, CPGL-B. With computational analysis, CPGL was located at chromosome 18q22.3 and was a homologue of peptidase family M20. CPGL was expressed in all adult and fetal tissues, whereas its isoform, CPGL-B, lacking exons 3 and 4, was expressed in all fetal tissues but only in liver and placenta of adult tissues. In HCC, CPGL-B was frequently underexpressed (35 of 90, 38.9%) in tumorous tissues compared with the corresponding nontumorous livers. Intriguingly, the underexpression was significantly associated with the presence of venous invasion (P = 0.018) and tumor microsatellite formation (P = 0.004). Stable transfection of CPGL-B in SMMC7721 HCC cells showed significant inhibition in cell viability, colony formation, cell invasion, and tumor formation in nude mice. CPGL-B also down-regulated CXCR3, matrix metalloproteinase 11, and CD44s, which are involved in cell growth and cell migration. Conclusions: These findings suggest that the frequent underexpression of CPGL-B may be associated with cell growth and metastasis of HCC. © 2006 American Association for Cancer Research.
 
ISSN1078-0432
2012 Impact Factor: 7.837
2012 SCImago Journal Rankings: 3.798
 
DOIhttp://dx.doi.org/10.1158/1078-0432.CCR-06-1307
 
ISI Accession Number IDWOS:000242263300006
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhang, P
 
dc.contributor.authorChan, DW
 
dc.contributor.authorYi, YZ
 
dc.contributor.authorJin, JL
 
dc.contributor.authorNg, IOL
 
dc.contributor.authorWan, D
 
dc.contributor.authorGu, J
 
dc.date.accessioned2010-09-06T09:45:21Z
 
dc.date.available2010-09-06T09:45:21Z
 
dc.date.issued2006
 
dc.description.abstractPurpose: We have previously done large-scale cDNA transfection screening on human hepatocellular carcinoma (HCC) cells and have identified 3,806 cDNA genes that possess the ability of either stimulating or inhibiting cell growth. In this study, we characterized one of these growth suppressor genes, carboxypeptidase of glutamate like-B (CPGL-B), in HCC. Experimental Design: Semiquantitative reverse-transcription PCR was used to examine the expression levels of CPGL-B. The cellular localization and functions of CPGL-B were investigated by enforced expression of CPGL-B in HCC cells. Results: From our previous cDNA transfection screening, we identified a gene named CPGL and its isoform, CPGL-B. With computational analysis, CPGL was located at chromosome 18q22.3 and was a homologue of peptidase family M20. CPGL was expressed in all adult and fetal tissues, whereas its isoform, CPGL-B, lacking exons 3 and 4, was expressed in all fetal tissues but only in liver and placenta of adult tissues. In HCC, CPGL-B was frequently underexpressed (35 of 90, 38.9%) in tumorous tissues compared with the corresponding nontumorous livers. Intriguingly, the underexpression was significantly associated with the presence of venous invasion (P = 0.018) and tumor microsatellite formation (P = 0.004). Stable transfection of CPGL-B in SMMC7721 HCC cells showed significant inhibition in cell viability, colony formation, cell invasion, and tumor formation in nude mice. CPGL-B also down-regulated CXCR3, matrix metalloproteinase 11, and CD44s, which are involved in cell growth and cell migration. Conclusions: These findings suggest that the frequent underexpression of CPGL-B may be associated with cell growth and metastasis of HCC. © 2006 American Association for Cancer Research.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationClinical Cancer Research, 2006, v. 12 n. 22, p. 6617-6625 [How to Cite?]
DOI: http://dx.doi.org/10.1158/1078-0432.CCR-06-1307
 
dc.identifier.doihttp://dx.doi.org/10.1158/1078-0432.CCR-06-1307
 
dc.identifier.epage6625
 
dc.identifier.hkuros129940
 
dc.identifier.isiWOS:000242263300006
 
dc.identifier.issn1078-0432
2012 Impact Factor: 7.837
2012 SCImago Journal Rankings: 3.798
 
dc.identifier.issue22
 
dc.identifier.openurl
 
dc.identifier.pmid17121880
 
dc.identifier.scopuseid_2-s2.0-33845290581
 
dc.identifier.spage6617
 
dc.identifier.urihttp://hdl.handle.net/10722/88588
 
dc.identifier.volume12
 
dc.languageeng
 
dc.publisherAmerican Association for Cancer Research.
 
dc.publisher.placeUnited States
 
dc.relation.ispartofClinical Cancer Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAmino Acid Sequence
 
dc.subject.meshAnimals
 
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathology - therapy
 
dc.subject.meshCell Survival
 
dc.subject.meshCells, Cultured
 
dc.subject.meshCytoplasm - metabolism
 
dc.subject.meshDipeptidases - genetics - isolation & purification - physiology
 
dc.subject.meshFemale
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshGrowth Inhibitors - isolation & purification
 
dc.subject.meshHumans
 
dc.subject.meshLiver - metabolism
 
dc.subject.meshLiver Neoplasms - metabolism - pathology - therapy
 
dc.subject.meshMice
 
dc.subject.meshMice, Inbred BALB C
 
dc.subject.meshMice, Nude
 
dc.subject.meshMolecular Sequence Data
 
dc.subject.meshNeoplasm Invasiveness
 
dc.subject.meshNeoplasm Metastasis - prevention & control
 
dc.subject.meshSequence Homology, Amino Acid
 
dc.subject.meshTissue Distribution
 
dc.subject.meshTransfection - methods
 
dc.subject.meshXenograft Model Antitumor Assays
 
dc.titleIdentification of carboxypeptidase of glutamate like-B as a candidate suppressor in cell growth and metastasis in human hepatocellular carcinoma
 
dc.typeArticle
 
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<contributor.author>Jin, JL</contributor.author>
<contributor.author>Ng, IOL</contributor.author>
<contributor.author>Wan, D</contributor.author>
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Author Affiliations
  1. The University of Hong Kong
  2. Shanghai Jiaotong University