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Article: Overexpression of GPR39 contributes to malignant development of human esophageal squamous cell carcinoma
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TitleOverexpression of GPR39 contributes to malignant development of human esophageal squamous cell carcinoma
 
AuthorsXie, F3
Liu, H3
Zhu, YH3
Qin, YR4
Dai, Y3
Zeng, T3
Chen, L1
Nie, C3
Tang, H2
Li, Y3
Fu, L3 1
Guan, XY3 1
 
Issue Date2011
 
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
 
CitationBmc Cancer, 2011, v. 11 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1471-2407-11-86
 
AbstractBackground: By using cDNA microarray analysis, we identified a G protein-coupled receptor, GPR39, that is significantly up-regulated in ESCC. The aim of this study is to investigate the role of GPR39 in human esophageal cancer development, and to examine the prevalence and clinical significance of GPR39 overexpression in ESCC.Methods: The mRNA expression level of GPR39 was analyzed in 9 ESCC cell lines and 50 primary ESCC tumors using semi-quantitative RT-PCR. Immunohistochemistry was used to assess GPR39 protein expression in tissue arrays containing 300 primary ESCC cases. In vitro and in vivo studies were done to elucidate the tumorigenic role of GPR39 in ESCC cells.Results: We found that GPR39 was frequently overexpressed in primary ESCCs in both mRNA level (27/50, 54%) and protein level (121/207, 58.5%), which was significantly associated with the lymph node metastasis and advanced TNM stage (P < 0.01). Functional studies showed that GPR39 has a strong tumorigenic ability. Introduction of GPR39 gene into ESCC cell line KYSE30 could promote cell proliferation, increase foci formation, colony formation in soft agar, and tumor formation in nude mice. The mechanism by which amplified GPR39 induces tumorigenesis was associated with its role in promoting G1/S transition via up-regulation of cyclin D1 and CDK6. Further study found GPR39 could enhance cell motility and invasiveness by inducing EMT and remodeling cytoskeleton. Moreover, depletion of endogenous GPR39 by siRNA could effectively decrease the oncogenicity of ESCC cells.Conclusions: The present study suggests that GPR39 plays an important tumorigenic role in the development and progression of ESCC. © 2011 Xie et al; licensee BioMed Central Ltd.
 
ISSN1471-2407
2012 Impact Factor: 3.333
2012 SCImago Journal Rankings: 1.331
 
DOIhttp://dx.doi.org/10.1186/1471-2407-11-86
 
PubMed Central IDPMC3053269
 
ISI Accession Number IDWOS:000288181800001
Funding AgencyGrant Number
National Natural Science Foundation of China30772475
30700820
30971606
Sun Yat-Sen University85000-3171311
Major State Basic Research Program of China2006CB910104
Research Fund for the Doctoral Program of Higher Education of China20070558272
Research Grant Council Central AllocationHKUST 2/06C
Funding Information:

This work was supported by Grants from National Natural Science Foundation of China (30772475, 30700820 and 30971606), Sun Yat-Sen University "Hundred Talents Program" (85000-3171311), Grant from the Major State Basic Research Program of China (2006CB910104), Research Fund for the Doctoral Program of Higher Education of China (20070558272) and Research Grant Council Central Allocation (HKUST 2/06C).

 
ReferencesReferences in Scopus
 
GrantsEsophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
Esophageal Carcinoma Research Center
 
DC FieldValue
dc.contributor.authorXie, F
 
dc.contributor.authorLiu, H
 
dc.contributor.authorZhu, YH
 
dc.contributor.authorQin, YR
 
dc.contributor.authorDai, Y
 
dc.contributor.authorZeng, T
 
dc.contributor.authorChen, L
 
dc.contributor.authorNie, C
 
dc.contributor.authorTang, H
 
dc.contributor.authorLi, Y
 
dc.contributor.authorFu, L
 
dc.contributor.authorGuan, XY
 
dc.date.accessioned2011-08-26T14:22:07Z
 
dc.date.available2011-08-26T14:22:07Z
 
dc.date.issued2011
 
dc.description.abstractBackground: By using cDNA microarray analysis, we identified a G protein-coupled receptor, GPR39, that is significantly up-regulated in ESCC. The aim of this study is to investigate the role of GPR39 in human esophageal cancer development, and to examine the prevalence and clinical significance of GPR39 overexpression in ESCC.Methods: The mRNA expression level of GPR39 was analyzed in 9 ESCC cell lines and 50 primary ESCC tumors using semi-quantitative RT-PCR. Immunohistochemistry was used to assess GPR39 protein expression in tissue arrays containing 300 primary ESCC cases. In vitro and in vivo studies were done to elucidate the tumorigenic role of GPR39 in ESCC cells.Results: We found that GPR39 was frequently overexpressed in primary ESCCs in both mRNA level (27/50, 54%) and protein level (121/207, 58.5%), which was significantly associated with the lymph node metastasis and advanced TNM stage (P < 0.01). Functional studies showed that GPR39 has a strong tumorigenic ability. Introduction of GPR39 gene into ESCC cell line KYSE30 could promote cell proliferation, increase foci formation, colony formation in soft agar, and tumor formation in nude mice. The mechanism by which amplified GPR39 induces tumorigenesis was associated with its role in promoting G1/S transition via up-regulation of cyclin D1 and CDK6. Further study found GPR39 could enhance cell motility and invasiveness by inducing EMT and remodeling cytoskeleton. Moreover, depletion of endogenous GPR39 by siRNA could effectively decrease the oncogenicity of ESCC cells.Conclusions: The present study suggests that GPR39 plays an important tumorigenic role in the development and progression of ESCC. © 2011 Xie et al; licensee BioMed Central Ltd.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationBmc Cancer, 2011, v. 11 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1471-2407-11-86
 
dc.identifier.citeulike8895393
 
dc.identifier.doihttp://dx.doi.org/10.1186/1471-2407-11-86
 
dc.identifier.hkuros190587
 
dc.identifier.isiWOS:000288181800001
Funding AgencyGrant Number
National Natural Science Foundation of China30772475
30700820
30971606
Sun Yat-Sen University85000-3171311
Major State Basic Research Program of China2006CB910104
Research Fund for the Doctoral Program of Higher Education of China20070558272
Research Grant Council Central AllocationHKUST 2/06C
Funding Information:

This work was supported by Grants from National Natural Science Foundation of China (30772475, 30700820 and 30971606), Sun Yat-Sen University "Hundred Talents Program" (85000-3171311), Grant from the Major State Basic Research Program of China (2006CB910104), Research Fund for the Doctoral Program of Higher Education of China (20070558272) and Research Grant Council Central Allocation (HKUST 2/06C).

 
dc.identifier.issn1471-2407
2012 Impact Factor: 3.333
2012 SCImago Journal Rankings: 1.331
 
dc.identifier.pmcidPMC3053269
 
dc.identifier.pmid21352519
 
dc.identifier.scopuseid_2-s2.0-79951958514
 
dc.identifier.urihttp://hdl.handle.net/10722/137267
 
dc.identifier.volume11
 
dc.languageeng
 
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofBMC Cancer
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.projectEsophageal Carcinoma Research Center
 
dc.relation.referencesReferences in Scopus
 
dc.rightsBMC Cancer. Copyright © BioMed Central Ltd.
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - pathology
 
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolism - pathology
 
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathology
 
dc.subject.meshReceptors, G-Protein-Coupled - genetics - metabolism - physiology
 
dc.subject.meshTransplantation, Heterologous
 
dc.titleOverexpression of GPR39 contributes to malignant development of human esophageal squamous cell carcinoma
 
dc.typeArticle
 
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<contributor.author>Dai, Y</contributor.author>
<contributor.author>Zeng, T</contributor.author>
<contributor.author>Chen, L</contributor.author>
<contributor.author>Nie, C</contributor.author>
<contributor.author>Tang, H</contributor.author>
<contributor.author>Li, Y</contributor.author>
<contributor.author>Fu, L</contributor.author>
<contributor.author>Guan, XY</contributor.author>
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<description.abstract>Background: By using cDNA microarray analysis, we identified a G protein-coupled receptor, GPR39, that is significantly up-regulated in ESCC. The aim of this study is to investigate the role of GPR39 in human esophageal cancer development, and to examine the prevalence and clinical significance of GPR39 overexpression in ESCC.Methods: The mRNA expression level of GPR39 was analyzed in 9 ESCC cell lines and 50 primary ESCC tumors using semi-quantitative RT-PCR. Immunohistochemistry was used to assess GPR39 protein expression in tissue arrays containing 300 primary ESCC cases. In vitro and in vivo studies were done to elucidate the tumorigenic role of GPR39 in ESCC cells.Results: We found that GPR39 was frequently overexpressed in primary ESCCs in both mRNA level (27/50, 54%) and protein level (121/207, 58.5%), which was significantly associated with the lymph node metastasis and advanced TNM stage (P &lt; 0.01). Functional studies showed that GPR39 has a strong tumorigenic ability. Introduction of GPR39 gene into ESCC cell line KYSE30 could promote cell proliferation, increase foci formation, colony formation in soft agar, and tumor formation in nude mice. The mechanism by which amplified GPR39 induces tumorigenesis was associated with its role in promoting G1/S transition via up-regulation of cyclin D1 and CDK6. Further study found GPR39 could enhance cell motility and invasiveness by inducing EMT and remodeling cytoskeleton. Moreover, depletion of endogenous GPR39 by siRNA could effectively decrease the oncogenicity of ESCC cells.Conclusions: The present study suggests that GPR39 plays an important tumorigenic role in the development and progression of ESCC. &#169; 2011 Xie et al; licensee BioMed Central Ltd.</description.abstract>
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<subject.mesh>Carcinoma, Squamous Cell - genetics - metabolism - pathology</subject.mesh>
<subject.mesh>Cell Transformation, Neoplastic - genetics - metabolism - pathology</subject.mesh>
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Author Affiliations
  1. The University of Hong Kong
  2. Zhengzhou University
  3. Sun Yat-Sen University
  4. First Affiliated Hospital of Zhengzhou University