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Article: Overexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma

TitleOverexpression of cathepsin Z contributes to tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma
Authors
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
Citation
Plos One, 2011, v. 6 n. 9 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/143735
ISSN
2014 Impact Factor: 3.234
2013 SCImago Journal Rankings: 1.724
PubMed Central ID
ISI Accession Number ID
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.

References
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DC FieldValueLanguage
dc.contributor.authorWang, Jen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2011-12-21T08:47:46Z-
dc.date.available2011-12-21T08:47:46Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 9en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/143735-
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.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
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 carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0024967en_HK
dc.identifier.pmid21966391-
dc.identifier.pmcidPMC3178578-
dc.identifier.scopuseid_2-s2.0-80053059111en_HK
dc.identifier.hkuros198002en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053059111&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue9en_HK
dc.identifier.isiWOS:000295265100035-
dc.publisher.placeUnited Statesen_HK
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.identifier.scopusauthoridWang, J=36078145500en_HK
dc.identifier.scopusauthoridChen, L=23569135400en_HK
dc.identifier.scopusauthoridLi, Y=36078298200en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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