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Article: Overexpression of EIF5A2 promotes colorectal carcinoma cell aggressiveness by upregulating MTA1 through C-myc to induce epithelial-mesenchymaltransition
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TitleOverexpression of EIF5A2 promotes colorectal carcinoma cell aggressiveness by upregulating MTA1 through C-myc to induce epithelial-mesenchymaltransition
 
AuthorsZhu, W2
Cai, MY2
Tong, ZT2
Dong, SS1
Mai, SJ2
Liao, YJ2
Bian, XW3
Lin, MC2 4
Kung, HF2 4
Zeng, YX2
Guan, XY2 1
Xie, D2
 
Issue Date2012
 
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
CitationGut, 2012, v. 61 n. 4, p. 562-575 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gutjnl-2011-300207
 
AbstractBACKGROUND AND AIMS: The authors have previously isolated a putative oncogene, eukaryotic initiation factor 5A2 (EIF5A2) from 3q26. In this study, EIF5A2 was characterised for its role in colorectal carcinoma (CRC) aggressiveness and underlying molecular mechanisms. METHODS: The expression dynamics of EIF5A2 were examined by immunohistochemistry in a cohort of carcinomatous and non-neoplastic colorectal tissues and cells. A series of in-vivo and in-vitro assays was performed to elucidate the function of EIF5A2 in CRC and its underlying mechanisms. RESULTS: The overexpression of EIF5A2 was examined by immunohistochemistry in 102/229 (44.5%) CRC patients, and it was significantly correlated with tumour metastasis and determined to be an independent predictor of shortened survival (p<0.05). Ectopic overexpression of EIF5A2 in CRC cells enhanced cell motility and invasion in vitro and tumour metastasis in vivo, and induced epithelial-mesenchymal transition (EMT). The depletion of EIF5A2 expression prevented CRC cell invasiveness and inhibited EMT. Importantly, the metastasis-associated protein 1 (MTA1) gene was identified as a potential downstream target of EIF5A2 in CRC cells, and knockdown of MTA1 eliminated the augmentation of carcinoma cell migration, invasion and EMT by ectopic EIF5A2. The overexpression of EIF5A2 in CRC cells substantially enhanced the enrichment of c-myc on the promoter of MTA1, and MTA1 upregulation by EIF5A2 was partly dependent on c-myc. CONCLUSION: The data suggest that EIF5A2 plays an important oncogenic role in CRC aggressiveness by the upregulation of MTA1 to induce EMT, and EIF5A2 could be employed as a novel prognostic marker and/or effective therapeutic target for CRC.
 
ISSN0017-5749
2013 Impact Factor: 13.319
 
DOIhttp://dx.doi.org/10.1136/gutjnl-2011-300207
 
ISI Accession Number IDWOS:000300955000014
Funding AgencyGrant Number
Nature Science Foundation of China30972884
973 Project of China2010CB529400
2010CB912802
Sun Yat-Sen University Cancer Center303045134001
Funding Information:

This work is supported by grants from the Nature Science Foundation of China (no 30972884), the 973 Project of China (2010CB529400 and 2010CB912802) and the Program for Excellent Young Talents in Sun Yat-Sen University Cancer Center (no 303045134001).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhu, W
 
dc.contributor.authorCai, MY
 
dc.contributor.authorTong, ZT
 
dc.contributor.authorDong, SS
 
dc.contributor.authorMai, SJ
 
dc.contributor.authorLiao, YJ
 
dc.contributor.authorBian, XW
 
dc.contributor.authorLin, MC
 
dc.contributor.authorKung, HF
 
dc.contributor.authorZeng, YX
 
dc.contributor.authorGuan, XY
 
dc.contributor.authorXie, D
 
dc.date.accessioned2012-06-26T06:12:35Z
 
dc.date.available2012-06-26T06:12:35Z
 
dc.date.issued2012
 
dc.description.abstractBACKGROUND AND AIMS: The authors have previously isolated a putative oncogene, eukaryotic initiation factor 5A2 (EIF5A2) from 3q26. In this study, EIF5A2 was characterised for its role in colorectal carcinoma (CRC) aggressiveness and underlying molecular mechanisms. METHODS: The expression dynamics of EIF5A2 were examined by immunohistochemistry in a cohort of carcinomatous and non-neoplastic colorectal tissues and cells. A series of in-vivo and in-vitro assays was performed to elucidate the function of EIF5A2 in CRC and its underlying mechanisms. RESULTS: The overexpression of EIF5A2 was examined by immunohistochemistry in 102/229 (44.5%) CRC patients, and it was significantly correlated with tumour metastasis and determined to be an independent predictor of shortened survival (p<0.05). Ectopic overexpression of EIF5A2 in CRC cells enhanced cell motility and invasion in vitro and tumour metastasis in vivo, and induced epithelial-mesenchymal transition (EMT). The depletion of EIF5A2 expression prevented CRC cell invasiveness and inhibited EMT. Importantly, the metastasis-associated protein 1 (MTA1) gene was identified as a potential downstream target of EIF5A2 in CRC cells, and knockdown of MTA1 eliminated the augmentation of carcinoma cell migration, invasion and EMT by ectopic EIF5A2. The overexpression of EIF5A2 in CRC cells substantially enhanced the enrichment of c-myc on the promoter of MTA1, and MTA1 upregulation by EIF5A2 was partly dependent on c-myc. CONCLUSION: The data suggest that EIF5A2 plays an important oncogenic role in CRC aggressiveness by the upregulation of MTA1 to induce EMT, and EIF5A2 could be employed as a novel prognostic marker and/or effective therapeutic target for CRC.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationGut, 2012, v. 61 n. 4, p. 562-575 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gutjnl-2011-300207
 
dc.identifier.citeulike11743477
 
dc.identifier.doihttp://dx.doi.org/10.1136/gutjnl-2011-300207
 
dc.identifier.epage575
 
dc.identifier.hkuros203482
 
dc.identifier.isiWOS:000300955000014
Funding AgencyGrant Number
Nature Science Foundation of China30972884
973 Project of China2010CB529400
2010CB912802
Sun Yat-Sen University Cancer Center303045134001
Funding Information:

This work is supported by grants from the Nature Science Foundation of China (no 30972884), the 973 Project of China (2010CB529400 and 2010CB912802) and the Program for Excellent Young Talents in Sun Yat-Sen University Cancer Center (no 303045134001).

 
dc.identifier.issn0017-5749
2013 Impact Factor: 13.319
 
dc.identifier.issue4
 
dc.identifier.pmid21813470
 
dc.identifier.scopuseid_2-s2.0-84857798740
 
dc.identifier.spage562
 
dc.identifier.urihttp://hdl.handle.net/10722/150854
 
dc.identifier.volume61
 
dc.languageeng
 
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofGut
 
dc.relation.referencesReferences in Scopus
 
dc.rightsGut. Copyright © BMJ Publishing Group.
 
dc.rightsThis article has been accepted for publication in [Gut]. The definitive copyedited, typeset version [Gut, 2012, v. 61 n. 4, p. 562-575] is available online at: www.gut.bmj.com
 
dc.subject.meshColorectal Neoplasms - metabolism - pathology
 
dc.subject.meshEpithelial-Mesenchymal Transition - physiology
 
dc.subject.meshHistone Deacetylases - biosynthesis
 
dc.subject.meshPeptide Initiation Factors - metabolism - physiology
 
dc.subject.meshRNA-Binding Proteins - metabolism - physiology
 
dc.titleOverexpression of EIF5A2 promotes colorectal carcinoma cell aggressiveness by upregulating MTA1 through C-myc to induce epithelial-mesenchymaltransition
 
dc.typeArticle
 
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<contributor.author>Tong, ZT</contributor.author>
<contributor.author>Dong, SS</contributor.author>
<contributor.author>Mai, SJ</contributor.author>
<contributor.author>Liao, YJ</contributor.author>
<contributor.author>Bian, XW</contributor.author>
<contributor.author>Lin, MC</contributor.author>
<contributor.author>Kung, HF</contributor.author>
<contributor.author>Zeng, YX</contributor.author>
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<description.abstract>BACKGROUND AND AIMS: The authors have previously isolated a putative oncogene, eukaryotic initiation factor 5A2 (EIF5A2) from 3q26. In this study, EIF5A2 was characterised for its role in colorectal carcinoma (CRC) aggressiveness and underlying molecular mechanisms. METHODS: The expression dynamics of EIF5A2 were examined by immunohistochemistry in a cohort of carcinomatous and non-neoplastic colorectal tissues and cells. A series of in-vivo and in-vitro assays was performed to elucidate the function of EIF5A2 in CRC and its underlying mechanisms. RESULTS: The overexpression of EIF5A2 was examined by immunohistochemistry in 102/229 (44.5%) CRC patients, and it was significantly correlated with tumour metastasis and determined to be an independent predictor of shortened survival (p&lt;0.05). Ectopic overexpression of EIF5A2 in CRC cells enhanced cell motility and invasion in vitro and tumour metastasis in vivo, and induced epithelial-mesenchymal transition (EMT). The depletion of EIF5A2 expression prevented CRC cell invasiveness and inhibited EMT. Importantly, the metastasis-associated protein 1 (MTA1) gene was identified as a potential downstream target of EIF5A2 in CRC cells, and knockdown of MTA1 eliminated the augmentation of carcinoma cell migration, invasion and EMT by ectopic EIF5A2. The overexpression of EIF5A2 in CRC cells substantially enhanced the enrichment of c-myc on the promoter of MTA1, and MTA1 upregulation by EIF5A2 was partly dependent on c-myc. CONCLUSION: The data suggest that EIF5A2 plays an important oncogenic role in CRC aggressiveness by the upregulation of MTA1 to induce EMT, and EIF5A2 could be employed as a novel prognostic marker and/or effective therapeutic target for CRC.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat-Sen University
  3. Third Military Medical University
  4. Chinese University of Hong Kong