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Article: Overexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma
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TitleOverexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma
 
AuthorsWang, J1
Chen, L1
Li, Y2
Guan, XY1 2
 
KeywordsCathepsin X
Amplicon
Carcinoma
Cell adhesion
Cell motility
 
Issue Date2011
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2011, v. 6 n. 9 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0024967
 
AbstractThe aim of this study was to characterize the oncogenic function and mechanism of Cathepsin Z (CTSZ) at 20q13.3, a frequently amplified region in hepatocellular carcinoma (HCC). Real-time PCR were used to compare CTSZ expression between paired HCC tumor and non-tumor specimens. CTSZ gene was stably transfected into HCC line QGY-7703 cells and its role in tumorigenicity and cell motility was characterized by soft agar, wound-healing, transwell invasion and cell adhesion assay, and tumor xenograft mouse model. Western blot analysis was used to study expression of proteins associated with epithelial-mesenchymal transition (EMT). Upregulation of CTSZ was detected in 59/137 (43%) of primary HCCs, which was significantly associated with advanced clinical stage (P = 0.000). Functional study found that CTSZ could increase colony formation in soft agar and promote cell motility. Further study found that the metastatic effect of CTSZ was associated with its role in inducing epithelial-mesenchymal transition (EMT) by upregulating mesenchymal markers (fibronectin and vimentin) and downregulating epithelial markers (E-cadherin and α-catenin). In addition, CTSZ could also upregulate proteins associated with extracellular matrix remodeling such as MMP2, MMP3 and MMP9. Taken together, our data suggested that CTSZ was a candidate oncogene within the 20q13 amplicon and it played an important role in HCC metastasis. © 2011 Wang et al.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0024967
 
PubMed Central IDPMC3178578
 
ISI Accession Number IDWOS:000295265100035
Funding AgencyGrant Number
Research Grant Council (RGC)HKUST 2/06C
HKU 7656/07M
HKU5/CRF/08
Major State Basic Research Program of China2006CB910104
Sun Yat-Sen University85000-3171311
Funding Information:

This work was funded by the Research Grant Council (RGC) Central Allocation (HKUST 2/06C), RGC Competitive Earmarked Research Grant (HKU 7656/07M), RGC Collaborative Research Fund (HKU5/CRF/08), the Major State Basic Research Program of China (2006CB910104), and Sun Yat-Sen University "Hundred Talents Program'' (85000-3171311). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
ReferencesReferences in Scopus
 
GrantsEsophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Liver Transplantation Research Centre: A Multidisciplinary Study for Liver Graft Injury
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
 
DC FieldValue
dc.contributor.authorWang, J
 
dc.contributor.authorChen, L
 
dc.contributor.authorLi, Y
 
dc.contributor.authorGuan, XY
 
dc.date.accessioned2011-12-21T08:47:46Z
 
dc.date.available2011-12-21T08:47:46Z
 
dc.date.issued2011
 
dc.description.abstractThe aim of this study was to characterize the oncogenic function and mechanism of Cathepsin Z (CTSZ) at 20q13.3, a frequently amplified region in hepatocellular carcinoma (HCC). Real-time PCR were used to compare CTSZ expression between paired HCC tumor and non-tumor specimens. CTSZ gene was stably transfected into HCC line QGY-7703 cells and its role in tumorigenicity and cell motility was characterized by soft agar, wound-healing, transwell invasion and cell adhesion assay, and tumor xenograft mouse model. Western blot analysis was used to study expression of proteins associated with epithelial-mesenchymal transition (EMT). Upregulation of CTSZ was detected in 59/137 (43%) of primary HCCs, which was significantly associated with advanced clinical stage (P = 0.000). Functional study found that CTSZ could increase colony formation in soft agar and promote cell motility. Further study found that the metastatic effect of CTSZ was associated with its role in inducing epithelial-mesenchymal transition (EMT) by upregulating mesenchymal markers (fibronectin and vimentin) and downregulating epithelial markers (E-cadherin and α-catenin). In addition, CTSZ could also upregulate proteins associated with extracellular matrix remodeling such as MMP2, MMP3 and MMP9. Taken together, our data suggested that CTSZ was a candidate oncogene within the 20q13 amplicon and it played an important role in HCC metastasis. © 2011 Wang et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2011, v. 6 n. 9 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0024967
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0024967
 
dc.identifier.hkuros198002
 
dc.identifier.isiWOS:000295265100035
Funding AgencyGrant Number
Research Grant Council (RGC)HKUST 2/06C
HKU 7656/07M
HKU5/CRF/08
Major State Basic Research Program of China2006CB910104
Sun Yat-Sen University85000-3171311
Funding Information:

This work was funded by the Research Grant Council (RGC) Central Allocation (HKUST 2/06C), RGC Competitive Earmarked Research Grant (HKU 7656/07M), RGC Collaborative Research Fund (HKU5/CRF/08), the Major State Basic Research Program of China (2006CB910104), and Sun Yat-Sen University "Hundred Talents Program'' (85000-3171311). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue9
 
dc.identifier.pmcidPMC3178578
 
dc.identifier.pmid21966391
 
dc.identifier.scopuseid_2-s2.0-80053059111
 
dc.identifier.urihttp://hdl.handle.net/10722/143735
 
dc.identifier.volume6
 
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.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectLiver Transplantation Research Centre: A Multidisciplinary Study for Liver Graft Injury
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subjectCathepsin X
 
dc.subjectAmplicon
 
dc.subjectCarcinoma
 
dc.subjectCell adhesion
 
dc.subjectCell motility
 
dc.titleOverexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma
 
dc.typeArticle
 
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<description.abstract>The aim of this study was to characterize the oncogenic function and mechanism of Cathepsin Z (CTSZ) at 20q13.3, a frequently amplified region in hepatocellular carcinoma (HCC). Real-time PCR were used to compare CTSZ expression between paired HCC tumor and non-tumor specimens. CTSZ gene was stably transfected into HCC line QGY-7703 cells and its role in tumorigenicity and cell motility was characterized by soft agar, wound-healing, transwell invasion and cell adhesion assay, and tumor xenograft mouse model. Western blot analysis was used to study expression of proteins associated with epithelial-mesenchymal transition (EMT). Upregulation of CTSZ was detected in 59/137 (43%) of primary HCCs, which was significantly associated with advanced clinical stage (P = 0.000). Functional study found that CTSZ could increase colony formation in soft agar and promote cell motility. Further study found that the metastatic effect of CTSZ was associated with its role in inducing epithelial-mesenchymal transition (EMT) by upregulating mesenchymal markers (fibronectin and vimentin) and downregulating epithelial markers (E-cadherin and &#945;-catenin). In addition, CTSZ could also upregulate proteins associated with extracellular matrix remodeling such as MMP2, MMP3 and MMP9. Taken together, our data suggested that CTSZ was a candidate oncogene within the 20q13 amplicon and it played an important role in HCC metastasis. &#169; 2011 Wang et al.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat-Sen University