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Article: Transforming capacity of two novel genes JS-1 and JS-2 located in chromosome 5p and their overexpression in human esophageal squamous cell carcinoma

TitleTransforming capacity of two novel genes JS-1 and JS-2 located in chromosome 5p and their overexpression in human esophageal squamous cell carcinoma
Authors
KeywordsEsophageal squamous cell carcinoma
Gene over-expression
Transforming capacity
Tumorigenicity
Issue Date2006
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htm
Citation
International Journal Of Molecular Medicine, 2006, v. 17 n. 1, p. 159-170 How to Cite?
AbstractEsophageal squamous cell carcinoma (ESCC) has a high mortality rate and geographic differences in incidence. Previous studies of comparative genomic hybridization (CGH) showed that chromosomal 5p is frequently amplified in cell lines and primary ESCC of Hong Kong Chinese origin. In this report, attempt was made to study two novel genes, named as JS-1 and JS-2, which are located in chromosome 5p15.2 and are 5′ upstream to δ catenin for their roles in molecular pathogenesis of ESCC. Eleven cell lines, 27 primary ESCC cases and multiple human tissue cDNA panels (MTC) of digestive system were studied for the expression level of JS-1 and JS-2 by RT-PCR. The full-length cDNA sequences of JS-1 and JS-2 were determined from a non-tumor esophageal epithelial cell line by 3′ and 5′ rapid amplification of cDNA ends (RACE). The transforming capacity of JS-1 and JS-2 was also investigated by transfecting NIH 3T3 cells with the expression vector pcDNA3.1(-) cloned with the full coding sequences and it was followed by the study of foci formation of the transfected cells under confluence growth and the anchorage-independent growth in soft agar. Forty-five percent (5/11) and 18% (2/11) of the ESCC cell lines showed overexpression of JS-1 and JS-2 respectively, while 55% (15/27) and 14% (3/22) primary ESCC cases showed overexpression of JS-1 and JS-2 respectively. JS-1 overexpression was most common in patients with stage II ESCC (6/27; 22%) whereas JS-2 was only overexpressed in a dysplastic lesion (1/22; 4%) and stage III tumors (2/22; 9%). The expression levels of JS-1 and JS-2 are both low in normal esophageal tissues. Overexpression of JS-1 in NIH 3T3 cells caused foci formation in confluence growth and colony formation in soft agar but not for JS-2. A high grade sarcoma was formed in the athymic nude mice when NIH 3T3 cells overexpressing JS-1 were injected subcutaneously. Our results thus indicate that the frequent overexpression of JS-1 in ESCC and its transforming capacity in normal cells may play a critical role in the molecular pathogenesis of ESCC. The present study also forms the ground work for further identification of novel mechanisms of molecular carcinogenesis in ESCC and other cancers.
Persistent Identifierhttp://hdl.handle.net/10722/67341
ISSN
2015 Impact Factor: 2.348
2015 SCImago Journal Rankings: 0.868
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFatima, Sen_HK
dc.contributor.authorChui, CHen_HK
dc.contributor.authorTang, WKen_HK
dc.contributor.authorHui, KSen_HK
dc.contributor.authorAu, HWen_HK
dc.contributor.authorLi, WYen_HK
dc.contributor.authorWong, MMen_HK
dc.contributor.authorCheung, Fen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorLam, KYen_HK
dc.contributor.authorBeh, PSLen_HK
dc.contributor.authorWong, Jen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorHo, KPen_HK
dc.contributor.authorChan, ASCen_HK
dc.contributor.authorTang, JCOen_HK
dc.date.accessioned2010-09-06T05:54:15Z-
dc.date.available2010-09-06T05:54:15Z-
dc.date.issued2006en_HK
dc.identifier.citationInternational Journal Of Molecular Medicine, 2006, v. 17 n. 1, p. 159-170en_HK
dc.identifier.issn1107-3756en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67341-
dc.description.abstractEsophageal squamous cell carcinoma (ESCC) has a high mortality rate and geographic differences in incidence. Previous studies of comparative genomic hybridization (CGH) showed that chromosomal 5p is frequently amplified in cell lines and primary ESCC of Hong Kong Chinese origin. In this report, attempt was made to study two novel genes, named as JS-1 and JS-2, which are located in chromosome 5p15.2 and are 5′ upstream to δ catenin for their roles in molecular pathogenesis of ESCC. Eleven cell lines, 27 primary ESCC cases and multiple human tissue cDNA panels (MTC) of digestive system were studied for the expression level of JS-1 and JS-2 by RT-PCR. The full-length cDNA sequences of JS-1 and JS-2 were determined from a non-tumor esophageal epithelial cell line by 3′ and 5′ rapid amplification of cDNA ends (RACE). The transforming capacity of JS-1 and JS-2 was also investigated by transfecting NIH 3T3 cells with the expression vector pcDNA3.1(-) cloned with the full coding sequences and it was followed by the study of foci formation of the transfected cells under confluence growth and the anchorage-independent growth in soft agar. Forty-five percent (5/11) and 18% (2/11) of the ESCC cell lines showed overexpression of JS-1 and JS-2 respectively, while 55% (15/27) and 14% (3/22) primary ESCC cases showed overexpression of JS-1 and JS-2 respectively. JS-1 overexpression was most common in patients with stage II ESCC (6/27; 22%) whereas JS-2 was only overexpressed in a dysplastic lesion (1/22; 4%) and stage III tumors (2/22; 9%). The expression levels of JS-1 and JS-2 are both low in normal esophageal tissues. Overexpression of JS-1 in NIH 3T3 cells caused foci formation in confluence growth and colony formation in soft agar but not for JS-2. A high grade sarcoma was formed in the athymic nude mice when NIH 3T3 cells overexpressing JS-1 were injected subcutaneously. Our results thus indicate that the frequent overexpression of JS-1 in ESCC and its transforming capacity in normal cells may play a critical role in the molecular pathogenesis of ESCC. The present study also forms the ground work for further identification of novel mechanisms of molecular carcinogenesis in ESCC and other cancers.en_HK
dc.languageengen_HK
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htmen_HK
dc.relation.ispartofInternational Journal of Molecular Medicineen_HK
dc.subjectEsophageal squamous cell carcinomaen_HK
dc.subjectGene over-expressionen_HK
dc.subjectTransforming capacityen_HK
dc.subjectTumorigenicityen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCarcinoma, Squamous Cell - genetics - pathologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshChromosomes, Human, Pair 5en_HK
dc.subject.meshEsophageal Neoplasms - genetics - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNIH 3T3 Cellsen_HK
dc.subject.meshNeoplasm Proteins - genetics - metabolismen_HK
dc.subject.meshSequence Analysis, DNAen_HK
dc.titleTransforming capacity of two novel genes JS-1 and JS-2 located in chromosome 5p and their overexpression in human esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1107-3756&volume=17&issue=1&spage=159&epage=170&date=2006&atitle=Transforming+capacity+of+two+novel+genes+JS-1+and+JS-2+located+in+chromosome+5p+and+their+overexpression+in+human+esophageal+squamous+cell+carcinomaen_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailBeh, PSL: philipbeh@pathology.hku.hken_HK
dc.identifier.emailWong, J: jwong@hkucc.hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityBeh, PSL=rp00409en_HK
dc.identifier.authorityWong, J=rp00322en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid16328025en_HK
dc.identifier.scopuseid_2-s2.0-33644873362en_HK
dc.identifier.hkuros114707en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644873362&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue1en_HK
dc.identifier.spage159en_HK
dc.identifier.epage170en_HK
dc.identifier.isiWOS:000234194100021-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridFatima, S=8437472300en_HK
dc.identifier.scopusauthoridChui, CH=7102093724en_HK
dc.identifier.scopusauthoridTang, WK=36678351100en_HK
dc.identifier.scopusauthoridHui, KS=7103304771en_HK
dc.identifier.scopusauthoridAu, HW=55209545200en_HK
dc.identifier.scopusauthoridLi, WY=36680411000en_HK
dc.identifier.scopusauthoridWong, MM=12777171900en_HK
dc.identifier.scopusauthoridCheung, F=35073678200en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridLam, KY=7403657165en_HK
dc.identifier.scopusauthoridBeh, PSL=6603146797en_HK
dc.identifier.scopusauthoridWong, J=8049324500en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridHo, KP=7403581513en_HK
dc.identifier.scopusauthoridChan, ASC=12778594200en_HK
dc.identifier.scopusauthoridTang, JCO=14056850300en_HK

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