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http://purl.uniprot.org/citations/26800338http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26800338http://www.w3.org/2000/01/rdf-schema#comment"Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. MiR-382 has been found to have a decreased expression and the ability to suppress tumorigenesis in certain cancers. However, the role of miR-382 in CRC has not been sufficiently investigated. NR2F2 (also known as COUP-TFII), a member of the steroid/thyroid receptor superfamily, is often aberrantly activated in various tumors, but it is currently unclear whether NR2F2 may be a target of miR-382. In the present study, we investigated the role of miR-382 in CRC and identified the regulation of NR2F2 by miR-382. We observed that miR-382 was aberrantly downregulated in CRC. Transfection with miR-382 mimics impeded the growth, migration, and invasion of CRC cells. The direct binding of miR-382 to the 3' untranslated region (3' UTR) of NR2F2 was confirmed using a luciferase reporter gene assay. We showed that the relative expression levels of NR2F2 were significantly higher in CRC tissues compared with normal adjacent mucosa. A Kaplan-Meier analysis indicated that patients with high NR2F2 expression had a poor overall survival. Knockdown of NR2F2 inhibited CRC cell growth, migration, and invasion. Ectopic expression of NR2F2 mitigated miR-382 suppression of CRC cell proliferation, migration, and invasion. In conclusion, the present study describes a potential mechanism underlying a miR-382/NR2F2 link contributing to CRC development. Our results demonstrate that miR-382 represents a potential strategy against CRC. © 2016 Wiley Periodicals, Inc."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.org/dc/terms/identifier"doi:10.1002/mc.22466"xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Jiang H."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Shi J."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Song J."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Zhou B."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Huang M."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Han T."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/author"Qiao H."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/name"Mol Carcinog"xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/pages"2260-2267"xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/title"MiR-382 inhibits cell growth and invasion by targeting NR2F2 in colorectal cancer."xsd:string
http://purl.uniprot.org/citations/26800338http://purl.uniprot.org/core/volume"55"xsd:string
http://purl.uniprot.org/citations/26800338http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26800338
http://purl.uniprot.org/citations/26800338http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26800338
http://purl.uniprot.org/uniprot/#_F1D8R0-mappedCitation-26800338http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26800338
http://purl.uniprot.org/uniprot/#_P24468-mappedCitation-26800338http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26800338
http://purl.uniprot.org/uniprot/F1D8R0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26800338
http://purl.uniprot.org/uniprot/P24468http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26800338