{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004239690836736.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.3892/ijo.2018.4369"}},{"identifier":{"@type":"PMID","@value":"29658604"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Oncogenic miR-96-5p inhibits apoptosis by targeting the caspase-9 gene in hepatocellular carcinoma"}],"description":[{"notation":[{"@value":"The aberrant expression or alteration of microRNAs (miRNAs/miRs) contributes to the development and progression of cancer. In the present study, the functions of miR-96-5p in hepatocellular carcinoma (HCC) were investigated. It was identified that miR-96-5p expression was significantly upregulated in primary HCC tumors compared with their non-tumorous counterparts. A copy number gain was frequently observed at chromosomal region 7q32.2 in which the MIR96 locus is located, suggesting that gene amplification may be one of the mechanisms by which miR-96-5p expression is increased in HCC. Transfection of miR-96-5p mimic into HCC cells decreased the expression of CASP9, which encodes caspase-9, the essential initiator caspase in the mitochondrial apoptotic pathway, at the mRNA and protein levels. A putative binding site for miR-96-5p was identified in the CASP9 3'-untranslated region, and the results of a luciferase assay indicated that CASP9 is a potential direct target of miR-96-5p. The miR-96-5p mimic increased resistance to doxorubicin- and ultraviolet-induced apoptosis through the decrease in caspase-9 expression in HCC cells. Transfection of miR-96-5p inhibitor enhanced the cytotoxic effect of doxorubicin by increasing caspase-9 expression in the HCC cells, suggesting a synergistic effect between the miR-96-5p inhibitor and doxorubicin. In conclusion, the results of the present study suggest that miR-96-5p, which is frequently upregulated in HCC, inhibits apoptosis by targeting CASP9. Therefore, miR-96-5p may be a potential therapeutic target for HCC."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1420564276181223424","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"00823270"},{"@type":"NRID","@value":"1000000823270"},{"@type":"NRID","@value":"9000413254259"},{"@type":"NRID","@value":"9000259834022"},{"@type":"NRID","@value":"9000403548897"},{"@type":"NRID","@value":"9000411390569"},{"@type":"NRID","@value":"9000396151481"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/iwainaoto"}],"foaf:name":[{"@value":"Naoto Iwai"}],"jpcoar:affiliationName":[{"@value":"Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, 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