Cited 182 times in
Genomic loss of miR-486 regulates tumor progression and the OLFM4 antiapoptotic factor in gastric cancer.
DC Field | Value | Language |
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dc.contributor.author | 라선영 | - |
dc.date.accessioned | 2014-12-20T17:49:10Z | - |
dc.date.available | 2014-12-20T17:49:10Z | - |
dc.date.issued | 2011 | - |
dc.identifier.issn | 1078-0432 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/95313 | - |
dc.description.abstract | PURPOSE: 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.statementOfResponsibility | open | - |
dc.format.extent | 2657~2667 | - |
dc.relation.isPartOf | CLINICAL CANCER RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Apoptosis/genetics | - |
dc.subject.MESH | Apoptosis Regulatory Proteins/genetics | - |
dc.subject.MESH | Apoptosis Regulatory Proteins/metabolism | - |
dc.subject.MESH | Carcinoma/genetics* | - |
dc.subject.MESH | Carcinoma/pathology | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cell Proliferation | - |
dc.subject.MESH | Disease Progression | - |
dc.subject.MESH | Gene Deletion* | - |
dc.subject.MESH | Gene Expression Profiling | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic | - |
dc.subject.MESH | Genes, Tumor Suppressor | - |
dc.subject.MESH | Genomic Instability/genetics | - |
dc.subject.MESH | Genomic Instability/physiology | - |
dc.subject.MESH | Granulocyte Colony-Stimulating Factor/genetics* | - |
dc.subject.MESH | Granulocyte Colony-Stimulating Factor/metabolism | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | MicroRNAs/genetics | - |
dc.subject.MESH | MicroRNAs/physiology* | - |
dc.subject.MESH | Microarray Analysis | - |
dc.subject.MESH | Neoplasms/genetics | - |
dc.subject.MESH | Neoplasms/pathology | - |
dc.subject.MESH | Stomach Neoplasms/genetics* | - |
dc.subject.MESH | Stomach Neoplasms/pathology | - |
dc.title | Genomic loss of miR-486 regulates tumor progression and the OLFM4 antiapoptotic factor in gastric cancer. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Hue-Kian Oh | - |
dc.contributor.googleauthor | Angie Lay-Keng Tan | - |
dc.contributor.googleauthor | Kakoli Das | - |
dc.contributor.googleauthor | Chia-Huey Ooi | - |
dc.contributor.googleauthor | Nian-Tao Deng | - |
dc.contributor.googleauthor | , Iain BeeHuat Tan | - |
dc.contributor.googleauthor | Emmanuel Beillard | - |
dc.contributor.googleauthor | Julian Lee | - |
dc.contributor.googleauthor | Kalpana Ramnarayanan | - |
dc.contributor.googleauthor | Sun-Young Rha | - |
dc.identifier.doi | 10.1158/1078-0432.CCR-10-3152 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01316 | - |
dc.relation.journalcode | J00564 | - |
dc.identifier.pmid | 21415212 | - |
dc.contributor.alternativeName | Rha, Sun Young | - |
dc.contributor.affiliatedAuthor | Rha, Sun Young | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 17 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 2657 | - |
dc.citation.endPage | 2667 | - |
dc.identifier.bibliographicCitation | CLINICAL CANCER RESEARCH, Vol.17(9) : 2657-2667, 2011 | - |
dc.identifier.rimsid | 31398 | - |
dc.type.rims | ART | - |
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