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Article: Four-and-a-half LIM protein 2 promotes invasive potential and epithelial-mesenchymal transition in colon cancer
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TitleFour-and-a-half LIM protein 2 promotes invasive potential and epithelial-mesenchymal transition in colon cancer
 
AuthorsZhang, W1 2
Jiang, B1
Guo, Z1
Sardet, C3
Zou, B2
Lam, CSC2
Li, J1
He, M4
Lan, HY2
Pang, R2
Hung, IFN2
Tan, VPY2
Wang, J1 2
Wong, BC2
 
Issue Date2010
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2010, v. 31 n. 7, p. 1220-1229 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgq094
 
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.
 
ISSN0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
DOIhttp://dx.doi.org/10.1093/carcin/bgq094
 
ISI Accession Number IDWOS:000279473100007
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhang, W
 
dc.contributor.authorJiang, B
 
dc.contributor.authorGuo, Z
 
dc.contributor.authorSardet, C
 
dc.contributor.authorZou, B
 
dc.contributor.authorLam, CSC
 
dc.contributor.authorLi, J
 
dc.contributor.authorHe, M
 
dc.contributor.authorLan, HY
 
dc.contributor.authorPang, R
 
dc.contributor.authorHung, IFN
 
dc.contributor.authorTan, VPY
 
dc.contributor.authorWang, J
 
dc.contributor.authorWong, BC
 
dc.date.accessioned2010-10-31T11:04:03Z
 
dc.date.available2010-10-31T11:04:03Z
 
dc.date.issued2010
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationCarcinogenesis, 2010, v. 31 n. 7, p. 1220-1229 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgq094
 
dc.identifier.citeulike7490447
 
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgq094
 
dc.identifier.epage1229
 
dc.identifier.hkuros174511
 
dc.identifier.isiWOS:000279473100007
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.

 
dc.identifier.issn0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
dc.identifier.issue7
 
dc.identifier.openurl
 
dc.identifier.pmid20460358
 
dc.identifier.scopuseid_2-s2.0-77954380650
 
dc.identifier.spage1220
 
dc.identifier.urihttp://hdl.handle.net/10722/124966
 
dc.identifier.volume31
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCarcinogenesis
 
dc.relation.referencesReferences in Scopus
 
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 cancer
 
dc.typeArticle
 
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<contributor.author>Sardet, C</contributor.author>
<contributor.author>Zou, B</contributor.author>
<contributor.author>Lam, CSC</contributor.author>
<contributor.author>Li, J</contributor.author>
<contributor.author>He, M</contributor.author>
<contributor.author>Lan, HY</contributor.author>
<contributor.author>Pang, R</contributor.author>
<contributor.author>Hung, IFN</contributor.author>
<contributor.author>Tan, VPY</contributor.author>
<contributor.author>Wang, J</contributor.author>
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<description.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 &#946;-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)-&#946;1. 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-&#946; signal mediators) in FHL2 stable transfectant cells. Therefore, FHL2 induced EMT in a TGF-&#946;-dependent and Smad-independent manner. FHL2 downregulated E-cadherin expression and inhibited the formation of membrane-associated E-cadherin-&#946;-catenin complex. FHL2 also stabilized nuclear &#946;-catenin, resulting in enforcement of &#946;-catenin transactivation activity. Conclusion: FHL2 is a potent EMT inducer and might be an important mediator for invasion and/or metastasis of colon cancer. &#169; The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.</description.abstract>
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Author Affiliations
  1. Southern Medical University
  2. The University of Hong Kong
  3. Universite Montpellier 1
  4. Chinese University of Hong Kong