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Article: Characterization of tumor-suppressive function of SOX6 in human esophageal squamous cell carcinoma

TitleCharacterization of tumor-suppressive function of SOX6 in human esophageal squamous cell carcinoma
Authors
KeywordsCancer growth
Cancer inhibition
Cancer staging
Cancer survival
Carcinogenesis
Issue Date2011
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2011, v. 17 n. 1, p. 46-55 How to Cite?
AbstractPurpose: By using cDNA microarray analysis, we identified a transcriptional factor, SOX6, was frequently downregulated in esophageal squamous cell carcinoma (ESCC). The aim of this study is to investigate the role of SOX6 in human esophageal cancer development, and to examine the prevalence and clinical significance of SOX6 downregulation in ESCC. Experimental Design: Expressions of SOX6 mRNA in 50 ESCCs and SOX6 protein in 300 ESCCs were investigated by semiquantitative RT-PCR and immunohistochemistry, respectively. The tumor-suppressive function of SOX6 was characterized by cell growth, foci formation, wound-healing and cell invasive assays, and tumor xenograft experiment. Western blot analysis was applied to detect protein expression levels. Results: SOX6 was frequently downregulated in primary ESCCs in both mRNA level (29/50, 58%) and protein level (149/219, 68.0%), which was significantly associated with the poor differentiation (P = 0.029), lymph node metastases (P = 0.014), advanced TNM stage (P = 0.000), and disease-specific survival (P < 0.001). Multivariate analysis indicated that the downregulation of SOX6 (P = 0.000) was a significant independent prognostic factors for ESCC. Functional studies showed that SOX6 was able to suppress both in vitro and in vivo tumorigenic ability of ESCC cells. The tumor-suppressive mechanism of SOX6 was associated with its role in G1/S cell-cycle arrest by upregulating expressions of p53 and p21 WAF1/CIP1 and downregulating expressions of cyclin D1/CDK4, cyclin A, and β-catenin. Conclusions: We provided the first evidence that SOX6 is a novel tumor-suppressor gene in ESCC development and is a potential prognostic marker in ESCC. ©2010 AACR.
Persistent Identifierhttp://hdl.handle.net/10722/137268
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
Funding AgencyGrant Number
Doctoral Program of Henan Province200703042
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:

Doctoral Program of Henan Province (200703042), National Natural Science Foundation of China (30772475, 30700820, and 30971606), Sun Yat-Sen University "Hundred Talents Program" (85000-3171311), 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).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorQin, YRen_HK
dc.contributor.authorTang, Hen_HK
dc.contributor.authorXie, Fen_HK
dc.contributor.authorLiu, Hen_HK
dc.contributor.authorZhu, Yen_HK
dc.contributor.authorAi, Jen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorKwong, DLen_HK
dc.contributor.authorFu, Len_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2011-08-26T14:22:09Z-
dc.date.available2011-08-26T14:22:09Z-
dc.date.issued2011en_HK
dc.identifier.citationClinical Cancer Research, 2011, v. 17 n. 1, p. 46-55en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137268-
dc.description.abstractPurpose: By using cDNA microarray analysis, we identified a transcriptional factor, SOX6, was frequently downregulated in esophageal squamous cell carcinoma (ESCC). The aim of this study is to investigate the role of SOX6 in human esophageal cancer development, and to examine the prevalence and clinical significance of SOX6 downregulation in ESCC. Experimental Design: Expressions of SOX6 mRNA in 50 ESCCs and SOX6 protein in 300 ESCCs were investigated by semiquantitative RT-PCR and immunohistochemistry, respectively. The tumor-suppressive function of SOX6 was characterized by cell growth, foci formation, wound-healing and cell invasive assays, and tumor xenograft experiment. Western blot analysis was applied to detect protein expression levels. Results: SOX6 was frequently downregulated in primary ESCCs in both mRNA level (29/50, 58%) and protein level (149/219, 68.0%), which was significantly associated with the poor differentiation (P = 0.029), lymph node metastases (P = 0.014), advanced TNM stage (P = 0.000), and disease-specific survival (P < 0.001). Multivariate analysis indicated that the downregulation of SOX6 (P = 0.000) was a significant independent prognostic factors for ESCC. Functional studies showed that SOX6 was able to suppress both in vitro and in vivo tumorigenic ability of ESCC cells. The tumor-suppressive mechanism of SOX6 was associated with its role in G1/S cell-cycle arrest by upregulating expressions of p53 and p21 WAF1/CIP1 and downregulating expressions of cyclin D1/CDK4, cyclin A, and β-catenin. Conclusions: We provided the first evidence that SOX6 is a novel tumor-suppressor gene in ESCC development and is a potential prognostic marker in ESCC. ©2010 AACR.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subjectCancer growth-
dc.subjectCancer inhibition-
dc.subjectCancer staging-
dc.subjectCancer survival-
dc.subjectCarcinogenesis-
dc.titleCharacterization of tumor-suppressive function of SOX6 in human esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=17&issue=1&spage=46&epage=55&date=2011&atitle=Characterization+of+tumor-suppressive+function+of+SOX6+in+human+esophageal+squamous+cell+carcinoma-
dc.identifier.emailKwong, DL:dlwkwong@hku.hken_HK
dc.identifier.emailFu, L:gracefu@graduate.hku.hken_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityKwong, DL=rp00414en_HK
dc.identifier.authorityFu, L=rp01435en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-10-1155en_HK
dc.identifier.pmid21084391-
dc.identifier.scopuseid_2-s2.0-78751496203en_HK
dc.identifier.hkuros190588en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78751496203&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue1en_HK
dc.identifier.spage46en_HK
dc.identifier.epage55en_HK
dc.identifier.eissn1557-3265-
dc.identifier.isiWOS:000285913600007-
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.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridQin, YR=7403100680en_HK
dc.identifier.scopusauthoridTang, H=36946431400en_HK
dc.identifier.scopusauthoridXie, F=22959384700en_HK
dc.identifier.scopusauthoridLiu, H=27171509500en_HK
dc.identifier.scopusauthoridZhu, Y=14322746600en_HK
dc.identifier.scopusauthoridAi, J=36945054600en_HK
dc.identifier.scopusauthoridChen, L=23569135400en_HK
dc.identifier.scopusauthoridLi, Y=35187394200en_HK
dc.identifier.scopusauthoridKwong, DL=15744231600en_HK
dc.identifier.scopusauthoridFu, L=22979236700en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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