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Article: Suppression of FHL2 Expression Induces Cell Differentiation and Inhibits Gastric and Colon Carcinogenesis

TitleSuppression of FHL2 Expression Induces Cell Differentiation and Inhibits Gastric and Colon Carcinogenesis
Authors
Issue Date2007
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 2007, v. 132 n. 3, p. 1066-1076 How to Cite?
AbstractBackground & Aims: FHL2 (4-1/2 LIM protein 2) is an adapter and modifier in protein interactions that is expressed mainly in the heart and ovary. It functions in a cell type- or promoter-specific manner. The aims of this study were to examine its expression in gastrointestinal cancers and to determine its role in cell differentiation and tumorigenesis. Methods: FHL2 expression in cancerous and normal gastrointestinal cells was detected by reverse-transcription polymerase chain reaction, immunoblotting, and immunohistochemistry. The effect of FHL2 suppression by both antisense and siRNA methods on cell differentiation and growth were evaluated in vitro and in vivo. Results: FHL2 expression was up-regulated in gastrointestinal cancer, compared with matched normal tissues. Stable transfection of gastric cancer cell line, AGS, and colon cancer cell line, Lovo, with antisense FHL2 induced lengthened or shuttle-shape morphologic changes with long or dendritic-like cytoplasmic processes and decreased the nuclear:cytoplasmic ratio. FHL2 antisense induced expressions of carinoembryonic antigen and E-cadherin and the maturation of F-actin. Furthermore, FHL2 antisense inhibited the transcriptions of some oncogenes including cox-2, survivin, c-jun, and hTERT, and suppressed the promoter activity of activator protein-1 and hTERT. Suppression of FHL2 inhibited serum-dependent, anchorage-dependent and -independent cell growth, and suppressed de novo tumor formation in nude mice xenograft. Conclusions: Suppression of FHL2 induces cell differentiation and inhibits tumorigenesis. Antisense or siRNA methods targeting FHL2 is a promising strategy for treatment of gastrointestinal cancers. © 2007 AGA Institute.
Persistent Identifierhttp://hdl.handle.net/10722/69635
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Jen_HK
dc.contributor.authorYang, Yen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorJiang, Ben_HK
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorLi, Gen_HK
dc.contributor.authorAn, Xen_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorZhuang, Zen_HK
dc.contributor.authorZhang, Zen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T06:15:28Z-
dc.date.available2010-09-06T06:15:28Z-
dc.date.issued2007en_HK
dc.identifier.citationGastroenterology, 2007, v. 132 n. 3, p. 1066-1076en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/69635-
dc.description.abstractBackground & Aims: FHL2 (4-1/2 LIM protein 2) is an adapter and modifier in protein interactions that is expressed mainly in the heart and ovary. It functions in a cell type- or promoter-specific manner. The aims of this study were to examine its expression in gastrointestinal cancers and to determine its role in cell differentiation and tumorigenesis. Methods: FHL2 expression in cancerous and normal gastrointestinal cells was detected by reverse-transcription polymerase chain reaction, immunoblotting, and immunohistochemistry. The effect of FHL2 suppression by both antisense and siRNA methods on cell differentiation and growth were evaluated in vitro and in vivo. Results: FHL2 expression was up-regulated in gastrointestinal cancer, compared with matched normal tissues. Stable transfection of gastric cancer cell line, AGS, and colon cancer cell line, Lovo, with antisense FHL2 induced lengthened or shuttle-shape morphologic changes with long or dendritic-like cytoplasmic processes and decreased the nuclear:cytoplasmic ratio. FHL2 antisense induced expressions of carinoembryonic antigen and E-cadherin and the maturation of F-actin. Furthermore, FHL2 antisense inhibited the transcriptions of some oncogenes including cox-2, survivin, c-jun, and hTERT, and suppressed the promoter activity of activator protein-1 and hTERT. Suppression of FHL2 inhibited serum-dependent, anchorage-dependent and -independent cell growth, and suppressed de novo tumor formation in nude mice xenograft. Conclusions: Suppression of FHL2 induces cell differentiation and inhibits tumorigenesis. Antisense or siRNA methods targeting FHL2 is a promising strategy for treatment of gastrointestinal cancers. © 2007 AGA Institute.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.subject.meshActins - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCadherins - metabolismen_HK
dc.subject.meshCarcinoembryonic Antigen - metabolismen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCell Shapeen_HK
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolism - pathologyen_HK
dc.subject.meshColonic Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshCyclooxygenase 2 - genetics - metabolismen_HK
dc.subject.meshHomeodomain Proteins - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Apoptosis Proteinsen_HK
dc.subject.meshLIM-Homeodomain Proteinsen_HK
dc.subject.meshMembrane Proteins - genetics - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMicrotubule-Associated Proteins - genetics - metabolismen_HK
dc.subject.meshMuscle Proteins - genetics - metabolismen_HK
dc.subject.meshNeoplasm Proteins - genetics - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-jun - genetics - metabolismen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA, Antisense - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshRNA, Small Interfering - metabolismen_HK
dc.subject.meshStomach Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshTelomerase - genetics - metabolismen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTranscription Factor AP-1 - metabolismen_HK
dc.subject.meshTranscription Factors - genetics - metabolismen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTransplantation, Heterologousen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleSuppression of FHL2 Expression Induces Cell Differentiation and Inhibits Gastric and Colon Carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=132&spage=1066&epage=1076&date=2007&atitle=Suppression+of+FHL2+Expression+Induces+Cell+Differentiation+and+Inhibits+Gastric+and+Colon+Carcinogenesis+en_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1053/j.gastro.2006.12.004en_HK
dc.identifier.pmid17383428-
dc.identifier.scopuseid_2-s2.0-33947321597en_HK
dc.identifier.hkuros142124en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33947321597&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume132en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1066en_HK
dc.identifier.epage1076en_HK
dc.identifier.isiWOS:000245182300029-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridYang, Y=8675011000en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridJiang, B=34770534200en_HK
dc.identifier.scopusauthoridPeng, Y=35249237100en_HK
dc.identifier.scopusauthoridLi, G=8692805500en_HK
dc.identifier.scopusauthoridAn, X=12774780700en_HK
dc.identifier.scopusauthoridZhang, Y=25923622400en_HK
dc.identifier.scopusauthoridZhuang, Z=7203003327en_HK
dc.identifier.scopusauthoridZhang, Z=8759618200en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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