File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: A microrna contribution to aberrant ras activation in gastric cancer
  • Basic View
  • Metadata View
  • XML View
TitleA microrna contribution to aberrant ras activation in gastric cancer
 
AuthorsLam, EKY4
Wang, X3
Shin, VY2
Zhang, S4
Morrison, H1
Sun, J3
Ng, EKO2
Yu, J4
Jin, H3
 
KeywordsEzrin
Gastric cancer
MiR-204
Ras
 
Issue Date2011
 
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.org
 
CitationAmerican Journal Of Translational Research, 2011, v. 3 n. 2, p. 209-218 [How to Cite?]
 
AbstractOncogenic Ras mutations are rare in gastric cancer, indicating that other mechanisms may be responsible for aberrant Ras activation in this type of cancer. Ezrin is critical to Ras activation by remodeling cortical actin cytoskeleton. In this study, we aimed to illustrate the relevance and regulation of ezrin in gastric cancer. Ezrin was upregulated in gastric cancer cells. Ezrin siRNA inhibited Ras activation, cell growth and cell migration. Ezrin overexpression was correlated with a poor outcome of gastric cancer patients (n=150, p<0.01). Cox regression analysis revealed a significant value of ezrin expression in prognosis prediction of gastric cancer (relative risk: 2.37, 95% confidence interval: 1.24-4.56, p<0.01). MiR-204, which was predicted to target ezrin, was downregulated in gastric cancer cells and gastric carcinomas (n=22, p<0.01). MiR-204 inhibited ezrin expression, Ras activation, cell growth and cell migration. Importantly, miR-204 suppressed the expression of luciferase controlled by wild-type but not mutated ezrin 3'-UTR. In conclusion, ezrin is important to Ras activation in gastric cancer. Its upregulation is an independent prognosis prediction factor for gastric cancer. By contributing to ezrin upregulation, miR-204 downregulation represents a novel mechanism for aberrant Ras activation in gastric carcinogenesis.
 
ISSN1943-8141
 
PubMed Central IDPMC3056566
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLam, EKY
 
dc.contributor.authorWang, X
 
dc.contributor.authorShin, VY
 
dc.contributor.authorZhang, S
 
dc.contributor.authorMorrison, H
 
dc.contributor.authorSun, J
 
dc.contributor.authorNg, EKO
 
dc.contributor.authorYu, J
 
dc.contributor.authorJin, H
 
dc.date.accessioned2011-07-27T01:37:11Z
 
dc.date.available2011-07-27T01:37:11Z
 
dc.date.issued2011
 
dc.description.abstractOncogenic Ras mutations are rare in gastric cancer, indicating that other mechanisms may be responsible for aberrant Ras activation in this type of cancer. Ezrin is critical to Ras activation by remodeling cortical actin cytoskeleton. In this study, we aimed to illustrate the relevance and regulation of ezrin in gastric cancer. Ezrin was upregulated in gastric cancer cells. Ezrin siRNA inhibited Ras activation, cell growth and cell migration. Ezrin overexpression was correlated with a poor outcome of gastric cancer patients (n=150, p<0.01). Cox regression analysis revealed a significant value of ezrin expression in prognosis prediction of gastric cancer (relative risk: 2.37, 95% confidence interval: 1.24-4.56, p<0.01). MiR-204, which was predicted to target ezrin, was downregulated in gastric cancer cells and gastric carcinomas (n=22, p<0.01). MiR-204 inhibited ezrin expression, Ras activation, cell growth and cell migration. Importantly, miR-204 suppressed the expression of luciferase controlled by wild-type but not mutated ezrin 3'-UTR. In conclusion, ezrin is important to Ras activation in gastric cancer. Its upregulation is an independent prognosis prediction factor for gastric cancer. By contributing to ezrin upregulation, miR-204 downregulation represents a novel mechanism for aberrant Ras activation in gastric carcinogenesis.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationAmerican Journal Of Translational Research, 2011, v. 3 n. 2, p. 209-218 [How to Cite?]
 
dc.identifier.epage218
 
dc.identifier.hkuros188344
 
dc.identifier.issn1943-8141
 
dc.identifier.issue2
 
dc.identifier.pmcidPMC3056566
 
dc.identifier.pmid21416062
 
dc.identifier.scopuseid_2-s2.0-79952921572
 
dc.identifier.spage209
 
dc.identifier.urihttp://hdl.handle.net/10722/135563
 
dc.identifier.volume3
 
dc.languageeng
 
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Translational Research
 
dc.relation.referencesReferences in Scopus
 
dc.subjectEzrin
 
dc.subjectGastric cancer
 
dc.subjectMiR-204
 
dc.subjectRas
 
dc.titleA microrna contribution to aberrant ras activation in gastric cancer
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Lam, EKY</contributor.author>
<contributor.author>Wang, X</contributor.author>
<contributor.author>Shin, VY</contributor.author>
<contributor.author>Zhang, S</contributor.author>
<contributor.author>Morrison, H</contributor.author>
<contributor.author>Sun, J</contributor.author>
<contributor.author>Ng, EKO</contributor.author>
<contributor.author>Yu, J</contributor.author>
<contributor.author>Jin, H</contributor.author>
<date.accessioned>2011-07-27T01:37:11Z</date.accessioned>
<date.available>2011-07-27T01:37:11Z</date.available>
<date.issued>2011</date.issued>
<identifier.citation>American Journal Of Translational Research, 2011, v. 3 n. 2, p. 209-218</identifier.citation>
<identifier.issn>1943-8141</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/135563</identifier.uri>
<description.abstract>Oncogenic Ras mutations are rare in gastric cancer, indicating that other mechanisms may be responsible for aberrant Ras activation in this type of cancer. Ezrin is critical to Ras activation by remodeling cortical actin cytoskeleton. In this study, we aimed to illustrate the relevance and regulation of ezrin in gastric cancer. Ezrin was upregulated in gastric cancer cells. Ezrin siRNA inhibited Ras activation, cell growth and cell migration. Ezrin overexpression was correlated with a poor outcome of gastric cancer patients (n=150, p&lt;0.01). Cox regression analysis revealed a significant value of ezrin expression in prognosis prediction of gastric cancer (relative risk: 2.37, 95% confidence interval: 1.24-4.56, p&lt;0.01). MiR-204, which was predicted to target ezrin, was downregulated in gastric cancer cells and gastric carcinomas (n=22, p&lt;0.01). MiR-204 inhibited ezrin expression, Ras activation, cell growth and cell migration. Importantly, miR-204 suppressed the expression of luciferase controlled by wild-type but not mutated ezrin 3&apos;-UTR. In conclusion, ezrin is important to Ras activation in gastric cancer. Its upregulation is an independent prognosis prediction factor for gastric cancer. By contributing to ezrin upregulation, miR-204 downregulation represents a novel mechanism for aberrant Ras activation in gastric carcinogenesis.</description.abstract>
<language>eng</language>
<publisher>E-Century Publishing Corporation. The Journal&apos;s web site is located at http://www.ajtr.org</publisher>
<relation.ispartof>American Journal of Translational Research</relation.ispartof>
<subject>Ezrin</subject>
<subject>Gastric cancer</subject>
<subject>MiR-204</subject>
<subject>Ras</subject>
<title>A microrna contribution to aberrant ras activation in gastric cancer</title>
<type>Article</type>
<description.nature>link_to_OA_fulltext</description.nature>
<identifier.pmid>21416062</identifier.pmid>
<identifier.pmcid>PMC3056566</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-79952921572</identifier.scopus>
<identifier.hkuros>188344</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-79952921572&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>3</identifier.volume>
<identifier.issue>2</identifier.issue>
<identifier.spage>209</identifier.spage>
<identifier.epage>218</identifier.epage>
<publisher.place>United States</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/135563/1/re01.htm</bitstream.url>
</item>
Author Affiliations
  1. Leibniz Institute for Age Research
  2. The University of Hong Kong
  3. Zhejiang University School of Medicine
  4. Chinese University of Hong Kong