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http://purl.uniprot.org/citations/31194576http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31194576http://www.w3.org/2000/01/rdf-schema#comment"Objectives: miR-200c-3p has been shown to serve as a tumor suppressor in various tumor types. However, the biological function of miR-200c-3p in nephroblastoma remains unknown. This study aims to investigate the biological function and regulatory mechanisms of miR-200c-3p in nephroblastoma development. Methods: The expression of miR-200c-3p in nephroblastoma tissues and cells was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of miR-200c-3p on the proliferation and cell cycle of SK-NEP-1 nephroblastoma cell line were evaluated by CCK-8 assay, colony formation assay, and flow cytometry. The effects of miR-200c-3p on the migratory and invasive capacities of SK-NEP-1 cells were measured by wound healing assay and transwell assay. The ability of miR-200c-3p to target fibroblast growth factor receptor substrate 2 (FRS2) was detected by quantitative PCR, western blot, and luciferase reporter assay. Results: The expression of miR-200c-3p was significantly downregulated in nephroblastoma tissues and cells compared with that in normal renal tissues and cells. miR-200c-3p inhibited the proliferative, migratory, and invasive capacities of nephroblastoma cells by targeting FRS2. Conclusions: miR-200c-3p suppresses the malignant behaviors of nephroblastoma cells by downregulating the expression of FRS2."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.org/dc/terms/identifier"doi:10.1089/bio.2019.0009"xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Li Z."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Li T."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Gu Q."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Wang C.C."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Zhao P."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/author"Wang Y.L."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/name"Biopreserv Biobank"xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/pages"444-451"xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/title"miR-200c-3p Suppresses the Proliferative, Migratory, and Invasive Capacities of Nephroblastoma Cells via Targeting FRS2."xsd:string
http://purl.uniprot.org/citations/31194576http://purl.uniprot.org/core/volume"17"xsd:string
http://purl.uniprot.org/citations/31194576http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31194576
http://purl.uniprot.org/citations/31194576http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31194576
http://purl.uniprot.org/uniprot/#_A0A384NQ31-mappedCitation-31194576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31194576
http://purl.uniprot.org/uniprot/#_L7RTG7-mappedCitation-31194576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31194576
http://purl.uniprot.org/uniprot/#_Q8WU20-mappedCitation-31194576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31194576
http://purl.uniprot.org/uniprot/Q8WU20http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31194576
http://purl.uniprot.org/uniprot/A0A384NQ31http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31194576
http://purl.uniprot.org/uniprot/L7RTG7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31194576