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Article: Four-and-a-half LIM protein 2 promotes invasive potential and epithelial-mesenchymal transition in colon cancer

TitleFour-and-a-half LIM protein 2 promotes invasive potential and epithelial-mesenchymal transition in colon cancer
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2010, v. 31 n. 7, p. 1220-1229 How to Cite?
Abstract
Background and Aims: Cancer invasion and metastasis may associate with the phenotype transition called epithelial-mesenchymal transition (EMT). We aim to evaluate the impact of four-and-ahalf LIM protein 2 (FHL2) on EMT and invasion of colon cancer. Methods: The functional role of FHL2 in EMT was determined by overexpression or small interfering RNA-mediated depletion of FHL2. Mechanisms of FHL2 on expression or activity of E-cadherin and β-catenin were assessed. Results: FHL2 was highly expressed in primary and metastatic colon cancer but not in normal tissues. FHL2 was critical for cancer cell adhesion to extracellular matrix, migration and invasion. FHL2 expression was stimulated by transforming growth factor (TGF)-β1. Moreover, FHL2 acted as a potent EMT inducer by stimulating vimentin and matrix metalloproteinase-9 expressions and causing a loss of E-cadherin, whereas those alterations of EMT markers were not affected by silencing of Smad molecules (typical TGF-β signal mediators) in FHL2 stable transfectant cells. Therefore, FHL2 induced EMT in a TGF-β-dependent and Smad-independent manner. FHL2 downregulated E-cadherin expression and inhibited the formation of membrane-associated E-cadherin-β-catenin complex. FHL2 also stabilized nuclear β-catenin, resulting in enforcement of β-catenin transactivation activity. Conclusion: FHL2 is a potent EMT inducer and might be an important mediator for invasion and/or metastasis of colon cancer. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.
Persistent Identifierhttp://hdl.handle.net/10722/124966
ISSN
2013 Impact Factor: 5.266
ISI Accession Number ID
Funding AgencyGrant Number
Simon KY Lee Gastroenterology Research Fund
National Natural Science Foundation of China30973404
Gordon Chiu stomach cancer research fund
University of Hong Kong
Research Grant Council of Hong Kong Special Administrative RegionHKU7785/09M
French Agence National de la recherche
Fondation pour la Recherche M'dicale to C.S.
Funding Information:

Simon KY Lee Gastroenterology Research Fund; National Natural Science Foundation of China (30973404); Gordon Chiu stomach cancer research fund; University of Hong Kong; Research Grant Council of Hong Kong Special Administrative Region (HKU7785/09M to Dr J.W.); French Agence National de la recherche, Fondation pour la Recherche M'dicale to C.S.

References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Wen_HK
dc.contributor.authorJiang, Ben_HK
dc.contributor.authorGuo, Zen_HK
dc.contributor.authorSardet, Cen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorLam, CSCen_HK
dc.contributor.authorLi, Jen_HK
dc.contributor.authorHe, Men_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorPang, Ren_HK
dc.contributor.authorHung, IFNen_HK
dc.contributor.authorTan, VPYen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorWong, BCen_HK
dc.date.accessioned2010-10-31T11:04:03Z-
dc.date.available2010-10-31T11:04:03Z-
dc.date.issued2010en_HK
dc.identifier.citationCarcinogenesis, 2010, v. 31 n. 7, p. 1220-1229en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124966-
dc.description.abstractBackground and Aims: Cancer invasion and metastasis may associate with the phenotype transition called epithelial-mesenchymal transition (EMT). We aim to evaluate the impact of four-and-ahalf LIM protein 2 (FHL2) on EMT and invasion of colon cancer. Methods: The functional role of FHL2 in EMT was determined by overexpression or small interfering RNA-mediated depletion of FHL2. Mechanisms of FHL2 on expression or activity of E-cadherin and β-catenin were assessed. Results: FHL2 was highly expressed in primary and metastatic colon cancer but not in normal tissues. FHL2 was critical for cancer cell adhesion to extracellular matrix, migration and invasion. FHL2 expression was stimulated by transforming growth factor (TGF)-β1. Moreover, FHL2 acted as a potent EMT inducer by stimulating vimentin and matrix metalloproteinase-9 expressions and causing a loss of E-cadherin, whereas those alterations of EMT markers were not affected by silencing of Smad molecules (typical TGF-β signal mediators) in FHL2 stable transfectant cells. Therefore, FHL2 induced EMT in a TGF-β-dependent and Smad-independent manner. FHL2 downregulated E-cadherin expression and inhibited the formation of membrane-associated E-cadherin-β-catenin complex. FHL2 also stabilized nuclear β-catenin, resulting in enforcement of β-catenin transactivation activity. Conclusion: FHL2 is a potent EMT inducer and might be an important mediator for invasion and/or metastasis of colon cancer. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.subject.meshColonic Neoplasms - pathology-
dc.subject.meshEpithelial Cells - pathology-
dc.subject.meshHomeodomain Proteins - analysis - physiology-
dc.subject.meshMesoderm - pathology-
dc.subject.meshMuscle Proteins - analysis - physiology-
dc.titleFour-and-a-half LIM protein 2 promotes invasive potential and epithelial-mesenchymal transition in colon canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=31&issue=7&spage=1220&epage=1229&date=2010&atitle=Four-and-a-half+LIM+protein+2+promotes+invasive+potential+and+epithelial-mesenchymal+transition+in+colon+canceren_HK
dc.identifier.emailPang, R: robertap@hku.hken_HK
dc.identifier.emailHung, IFN: ivanhung@hkucc.hku.hken_HK
dc.identifier.emailTan, VPY: vpytan@hku.hken_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailWong, BC: bcywong@hku.hken_HK
dc.identifier.authorityPang, R=rp00274en_HK
dc.identifier.authorityHung, IFN=rp00508en_HK
dc.identifier.authorityTan, VPY=rp01458en_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityWong, BC=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/carcin/bgq094en_HK
dc.identifier.pmid20460358en_HK
dc.identifier.scopuseid_2-s2.0-77954380650en_HK
dc.identifier.hkuros174511en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954380650&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1220en_HK
dc.identifier.epage1229en_HK
dc.identifier.isiWOS:000279473100007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhang, W=7409428339en_HK
dc.identifier.scopusauthoridJiang, B=34770534200en_HK
dc.identifier.scopusauthoridGuo, Z=36128552900en_HK
dc.identifier.scopusauthoridSardet, C=7005616535en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridLam, CSC=35332626500en_HK
dc.identifier.scopusauthoridLi, J=7410060376en_HK
dc.identifier.scopusauthoridHe, M=35080389700en_HK
dc.identifier.scopusauthoridLan, HY=24544799000en_HK
dc.identifier.scopusauthoridPang, R=7004376659en_HK
dc.identifier.scopusauthoridHung, IFN=7006103457en_HK
dc.identifier.scopusauthoridTan, VPY=24449627600en_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridWong, BC=7402023340en_HK
dc.identifier.citeulike7490447-

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