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Genomic loss of miR-486 regulates tumor progression and the OLFM4 antiapoptotic factor in gastric cancer.

DC FieldValueLanguage
dc.contributor.author라선영-
dc.date.accessioned2014-12-20T17:49:10Z-
dc.date.available2014-12-20T17:49:10Z-
dc.date.issued2011-
dc.identifier.issn1078-0432-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/95313-
dc.description.abstractPURPOSE: MicroRNAs (miRNA) play pivotal oncogenic and tumor-suppressor roles in several human cancers. We sought to discover novel tumor-suppressor miRNAs in gastric cancer (GC). EXPERIMENTAL DESIGN: Using Agilent miRNA microarrays, we compared miRNA expression profiles of 40 primary gastric tumors and 40 gastric normal tissues, identifying miRNAs significantly downregulated in gastric tumors. RESULTS: Among the top 80 miRNAs differentially expressed between gastric tumors and normals (false discovery rate < 0.01), we identified hsa-miR-486 (miR-486) as a significantly downregulated miRNA in primary GCs and GC cell lines. Restoration of miR-486 expression in GC cell lines (YCC3, SCH and AGS) caused suppression of several pro-oncogenic traits, whereas conversely inhibiting miR-486 expression in YCC6 GC cells enhanced cellular proliferation. Array-CGH analysis of 106 primary GCs revealed genomic loss of the miR-486 locus in approximately 25% to 30% of GCs, including two tumors with focal genomic losses specifically deleting miR-486, consistent with miR-486 playing a tumor-suppressive role. Bioinformatic analysis identified the secreted antiapoptotic glycoprotein OLFM4 as a potential miR-486 target. Restoring miR-486 expression in GC cells decreased endogenous OLFM4 transcript and protein levels, and also inhibited expression of luciferase reporters containing an OLFM4 3' untranslated region with predicted miR-486 binding sites. Supporting the biological relevance of OLFM4 as a miR-486 target, proliferation in GC cells was also significantly reduced by OLFM4 silencing. CONCLUSIONS: miR-486 may function as a novel tumor-suppressor miRNA in GC. Its antioncogenic activity may involve the direct targeting and inhibition of OLFM4.-
dc.description.statementOfResponsibilityopen-
dc.format.extent2657~2667-
dc.relation.isPartOfCLINICAL CANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/genetics-
dc.subject.MESHApoptosis Regulatory Proteins/genetics-
dc.subject.MESHApoptosis Regulatory Proteins/metabolism-
dc.subject.MESHCarcinoma/genetics*-
dc.subject.MESHCarcinoma/pathology-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Proliferation-
dc.subject.MESHDisease Progression-
dc.subject.MESHGene Deletion*-
dc.subject.MESHGene Expression Profiling-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHGenes, Tumor Suppressor-
dc.subject.MESHGenomic Instability/genetics-
dc.subject.MESHGenomic Instability/physiology-
dc.subject.MESHGranulocyte Colony-Stimulating Factor/genetics*-
dc.subject.MESHGranulocyte Colony-Stimulating Factor/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHMicroRNAs/genetics-
dc.subject.MESHMicroRNAs/physiology*-
dc.subject.MESHMicroarray Analysis-
dc.subject.MESHNeoplasms/genetics-
dc.subject.MESHNeoplasms/pathology-
dc.subject.MESHStomach Neoplasms/genetics*-
dc.subject.MESHStomach Neoplasms/pathology-
dc.titleGenomic loss of miR-486 regulates tumor progression and the OLFM4 antiapoptotic factor in gastric cancer.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorHue-Kian Oh-
dc.contributor.googleauthorAngie Lay-Keng Tan-
dc.contributor.googleauthorKakoli Das-
dc.contributor.googleauthorChia-Huey Ooi-
dc.contributor.googleauthorNian-Tao Deng-
dc.contributor.googleauthor, Iain BeeHuat Tan-
dc.contributor.googleauthorEmmanuel Beillard-
dc.contributor.googleauthorJulian Lee-
dc.contributor.googleauthorKalpana Ramnarayanan-
dc.contributor.googleauthorSun-Young Rha-
dc.identifier.doi10.1158/1078-0432.CCR-10-3152-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01316-
dc.relation.journalcodeJ00564-
dc.identifier.pmid21415212-
dc.contributor.alternativeNameRha, Sun Young-
dc.contributor.affiliatedAuthorRha, Sun Young-
dc.rights.accessRightsfree-
dc.citation.volume17-
dc.citation.number9-
dc.citation.startPage2657-
dc.citation.endPage2667-
dc.identifier.bibliographicCitationCLINICAL CANCER RESEARCH, Vol.17(9) : 2657-2667, 2011-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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