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http://purl.uniprot.org/citations/27120784http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27120784http://www.w3.org/2000/01/rdf-schema#comment"The miR-145-5p, which induces TP53-dependent apoptosis, is down-regulated in several tumors, including hepatocellular carcinomas (HCCs), but some HCCs show physiological expression of this miR. Here we demonstrate that in HCC cells carrying wild-type TP53 the steady activation of the miR-145 signaling selects clones resistant to apoptosis via up-regulation of the oncogenic miR-483-3p. Expression of the miR-145-5p and of the miR-483-3p correlated negatively in non-neoplastic liver (n=41; ρ=-0.342, P=0.028), but positively in HCCs (n=21; ρ=0.791, P<0.0001), which we hypothesized to be due to impaired glucose metabolism in HCCs versus normal liver. In fact, when liver cancer cells were grown in low glucose, miR-145-5p lowered miR-483-3p expression, allowing apoptosis, whereas when cells were grown in high glucose the levels of miR-483-3p increased, reducing the apoptotic rate. This indicates that depending on glucose availability the miR-145-5p has double effects on the miR-483-3p, either inhibitory or stimulatory. Moreover, resistance to apoptosis in clones overexpressing both miR-145-5p and miR-483-3p was abrogated by silencing the miR-483-3p. Our data highlight a novel mechanism of resistance to apoptosis in liver cancer cells harbouring wild type TP53 and suggest a potential role of miR-145-5p and miR-483-3p as druggable targets in a subset of HCCs."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.8913"xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Calin G.A."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Ferracin M."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Negrini M."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Sabbioni S."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Veronese A."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Mariani-Costantini R."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Visone R."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Lupini L."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Callegari E."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Lanuti P."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Ghasemi R."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Spizzo R."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Bolondi L."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Gramantieri L."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Fornari F."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Braconi C."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Zagatti B."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Pepe F."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/author"Pagotto S."xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/name"Oncotarget"xsd:string
http://purl.uniprot.org/citations/27120784http://purl.uniprot.org/core/pages"31361-31371"xsd:string