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Article: Oncogene functions of FHL2 are independent from NF-κBIα in gastrointestinal cancer

TitleOncogene functions of FHL2 are independent from NF-κBIα in gastrointestinal cancer
Authors
KeywordsColon cancer
FHL2
Gastric cancer
Interaction
NF-κB
NF-κBIα
Issue Date2009
Citation
Pathology And Oncology Research, 2009, v. 15 n. 1, p. 31-36 How to Cite?
AbstractFour and a half of LIM-only protein 2 (FHL2) is an adaptor protein that can interact with many transcription factors and thus plays a variety of biological functions. Previous studies by our group have demonstrated that suppression of FHL2 was capable of inducing tumor cell differentiation, and inhibiting the growth of experimental gastric and colon cancers. Therefore, FHL2 appears to function as an oncogene. In order to further explore the mechanisms of how FHL2 is involved in tumorigenesis, we attempted to test whether FHL2 has any direct association with nuclear factor (NF-κB), the most important transcription factor involved in apoptosis, inflammation, and carcinogenesis. Using an Yeast Two Hybrid (Y2H) screening system, we have shown that FHL2 may have an interaction with NF-κBIα, the coding gene for IκBα which is the most potent endogenous inhibitor for NF-κB activation. However, subsequent studies using co-immunoprecipitation and co-localization failed to confirm the Y2H finding. Down-regulation of FHL2 by FHL2-siRNA down-regulated the expression of NF-κB p65. We therefore concluded that under the physiological condition, FHL2 may activate NF-κB pathway, even though such an activation may not be mediated by a direct binding of FHL2 to NF-κB inhibitor protein IκB. © 2008 Arányi Lajos Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/59228
ISSN
2015 Impact Factor: 1.94
2015 SCImago Journal Rankings: 0.692
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQiao, Len_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorPang, Ren_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorDai, Yen_HK
dc.contributor.authorMa, Jen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorLi, Zen_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-05-31T03:45:39Z-
dc.date.available2010-05-31T03:45:39Z-
dc.date.issued2009en_HK
dc.identifier.citationPathology And Oncology Research, 2009, v. 15 n. 1, p. 31-36en_HK
dc.identifier.issn1219-4956en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59228-
dc.description.abstractFour and a half of LIM-only protein 2 (FHL2) is an adaptor protein that can interact with many transcription factors and thus plays a variety of biological functions. Previous studies by our group have demonstrated that suppression of FHL2 was capable of inducing tumor cell differentiation, and inhibiting the growth of experimental gastric and colon cancers. Therefore, FHL2 appears to function as an oncogene. In order to further explore the mechanisms of how FHL2 is involved in tumorigenesis, we attempted to test whether FHL2 has any direct association with nuclear factor (NF-κB), the most important transcription factor involved in apoptosis, inflammation, and carcinogenesis. Using an Yeast Two Hybrid (Y2H) screening system, we have shown that FHL2 may have an interaction with NF-κBIα, the coding gene for IκBα which is the most potent endogenous inhibitor for NF-κB activation. However, subsequent studies using co-immunoprecipitation and co-localization failed to confirm the Y2H finding. Down-regulation of FHL2 by FHL2-siRNA down-regulated the expression of NF-κB p65. We therefore concluded that under the physiological condition, FHL2 may activate NF-κB pathway, even though such an activation may not be mediated by a direct binding of FHL2 to NF-κB inhibitor protein IκB. © 2008 Arányi Lajos Foundation.en_HK
dc.languageengen_HK
dc.relation.ispartofPathology and Oncology Researchen_HK
dc.subjectColon canceren_HK
dc.subjectFHL2en_HK
dc.subjectGastric canceren_HK
dc.subjectInteractionen_HK
dc.subjectNF-κBen_HK
dc.subjectNF-κBIαen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshColonic Neoplasms - metabolism - pathologyen_HK
dc.subject.meshHomeodomain Proteins - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshI-kappa B Proteins - metabolismen_HK
dc.subject.meshImmunoprecipitationen_HK
dc.subject.meshLIM-Homeodomain Proteinsen_HK
dc.subject.meshMuscle Proteins - metabolismen_HK
dc.subject.meshNF-kappa Ben_HK
dc.subject.meshProtein Interaction Domains and Motifsen_HK
dc.subject.meshStomach Neoplasms - metabolism - pathologyen_HK
dc.subject.meshSubcellular Fractionsen_HK
dc.subject.meshTranscription Factors - metabolismen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTwo-Hybrid System Techniquesen_HK
dc.titleOncogene functions of FHL2 are independent from NF-κBIα in gastrointestinal canceren_HK
dc.typeArticleen_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailPang, R: robertap@hku.hken_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityPang, R=rp00274en_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12253-008-9085-1en_HK
dc.identifier.pmid18752053-
dc.identifier.scopuseid_2-s2.0-67749088536en_HK
dc.identifier.hkuros143052en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67749088536&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue1en_HK
dc.identifier.spage31en_HK
dc.identifier.epage36en_HK
dc.identifier.isiWOS:000265093600005-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridWang, Y=7601492022en_HK
dc.identifier.scopusauthoridPang, R=7004376659en_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridDai, Y=7401512993en_HK
dc.identifier.scopusauthoridMa, J=35275386200en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridLi, Z=24171072000en_HK
dc.identifier.scopusauthoridZhang, Y=36129128700en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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