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Article: The four-and-a-half-LIM protein 2 (FHL2) is overexpressed in gliomas and associated with oncogenic activities

TitleThe four-and-a-half-LIM protein 2 (FHL2) is overexpressed in gliomas and associated with oncogenic activities
Authors
KeywordsCell migration
Cell proliferation
FHL2
Glioma
Tumorigenesis
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37090
Citation
Glia, 2008, v. 56 n. 12, p. 1328-1338 How to Cite?
AbstractFour-and-a-half-LIM protein 2 (FHL2) is a member of FHL protein family, which plays a crucial role in regulating gene expression, cell survival, and migration. Although its function in oncogenesis appears to be tumor type-specific, its roles in glioma formation and development are yet to be elucidated. In the present study, we demonstrated that the mRNA level of FHL2 was elevated in both low- and high-grade glioma samples. Overexpression of FHL2 stimulated the proliferation, anchorage-independent growth, and migration of human glioblastoma cells. Conversely, FHL2 knockdown by short hairpin RNA (shRNA-FHL2) inhibited glioblastoma cell proliferation and migration. Overexpression of FHL2 increased the tumorigenicity of glioblastoma cells in nude mice and decreased the mRNA levels of p53 and its downstream proapoptotic genes, including p21, Bcl2-associated protein X (Bax), and p53-upregulated modulator of apoptosis. It also enhanced the promoter activities of activator protein-1 (AP-1), human telomerase reverse transcriptase, and survivin genes. Together, these results provide the first evidence that FHL2 contributes to glioma carcinogenesis. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/58452
ISSN
2015 Impact Factor: 5.997
2015 SCImago Journal Rankings: 3.296
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Men_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorChan, CYen_HK
dc.contributor.authorChen, ACen_HK
dc.contributor.authorXia, HPen_HK
dc.contributor.authorYew, DTen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorChen, Zen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLi, MCMen_HK
dc.date.accessioned2010-05-31T03:30:33Z-
dc.date.available2010-05-31T03:30:33Z-
dc.date.issued2008en_HK
dc.identifier.citationGlia, 2008, v. 56 n. 12, p. 1328-1338en_HK
dc.identifier.issn0894-1491en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58452-
dc.description.abstractFour-and-a-half-LIM protein 2 (FHL2) is a member of FHL protein family, which plays a crucial role in regulating gene expression, cell survival, and migration. Although its function in oncogenesis appears to be tumor type-specific, its roles in glioma formation and development are yet to be elucidated. In the present study, we demonstrated that the mRNA level of FHL2 was elevated in both low- and high-grade glioma samples. Overexpression of FHL2 stimulated the proliferation, anchorage-independent growth, and migration of human glioblastoma cells. Conversely, FHL2 knockdown by short hairpin RNA (shRNA-FHL2) inhibited glioblastoma cell proliferation and migration. Overexpression of FHL2 increased the tumorigenicity of glioblastoma cells in nude mice and decreased the mRNA levels of p53 and its downstream proapoptotic genes, including p21, Bcl2-associated protein X (Bax), and p53-upregulated modulator of apoptosis. It also enhanced the promoter activities of activator protein-1 (AP-1), human telomerase reverse transcriptase, and survivin genes. Together, these results provide the first evidence that FHL2 contributes to glioma carcinogenesis. © 2008 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37090en_HK
dc.relation.ispartofGLIAen_HK
dc.rightsGlia. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectCell migrationen_HK
dc.subjectCell proliferationen_HK
dc.subjectFHL2en_HK
dc.subjectGliomaen_HK
dc.subjectTumorigenesisen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolismen_HK
dc.subject.meshEnzyme Activation - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - physiologyen_HK
dc.subject.meshGlioblastoma - genetics - metabolismen_HK
dc.subject.meshGlioma - genetics - metabolismen_HK
dc.subject.meshHomeodomain Proteins - biosynthesis - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLIM-Homeodomain Proteinsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMuscle Proteins - biosynthesis - deficiency - geneticsen_HK
dc.subject.meshNeoplasm Proteins - biosynthesis - deficiency - geneticsen_HK
dc.subject.meshOncogenes - physiologyen_HK
dc.subject.meshRNA, Messenger - biosynthesis - geneticsen_HK
dc.subject.meshTranscription Factors - biosynthesis - deficiency - geneticsen_HK
dc.subject.meshTumor Suppressor Protein p53 - biosynthesis - geneticsen_HK
dc.subject.meshUp-Regulation - geneticsen_HK
dc.titleThe four-and-a-half-LIM protein 2 (FHL2) is overexpressed in gliomas and associated with oncogenic activitiesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0894-1491&volume=56&issue=12&spage=1328&epage=1338&date=2008&atitle=The+Four-and-a-half-LIM+Protein+2+(FHL2)+is+Overexpressed+in+Gliomas+and+Associated+with+Oncogenic+Activitiesen_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.emailLi, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.identifier.authorityLi, MCM=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/glia.20701en_HK
dc.identifier.pmid18615633-
dc.identifier.scopuseid_2-s2.0-51349099009en_HK
dc.identifier.hkuros145998en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51349099009&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume56en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1328en_HK
dc.identifier.epage1338en_HK
dc.identifier.isiWOS:000258419000007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, M=36067425800en_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridChan, CY=22033276600en_HK
dc.identifier.scopusauthoridChen, AC=55447357500en_HK
dc.identifier.scopusauthoridXia, HP=12545165300en_HK
dc.identifier.scopusauthoridYew, DT=7007034694en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridChen, Z=26643572800en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLi, MCM=7404816359en_HK

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