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http://purl.uniprot.org/citations/25426560http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25426560http://www.w3.org/2000/01/rdf-schema#comment"Although the combination of etoposide (VP16) and cisplatin (DDP) is widely used as a first-line treatment for advanced-stage small-cell lung cancer (SCLC), chemoresistance limits its clinical use. Abnormalities of autophagy are associated with tumor chemoresistance. The present study found that miR-24-3p, a recently discovered microRNA, is significantly downregulated in VP16-DDP-resistant SCLC cells (H446/EP) compared with VP16-DDP-sensitive parent cells (H446). Forced expression of miR-24-3p sensitized H446/EP cells to VP16-DDP treatment because of a blockade of autophagic activity. We further found that downregulated miR-24-3p enhanced autophagy activation as it directly targets and inhibits autophagy-associated gene 4A (ATG4A). Overexpression of miR-24-3p into H446/EP cells led to reduction of the ATG4A protein level, allowing SCLC cells to resensitize to VP16-DDP. We conclude that miR-24-3p regulates autophagy by targeting ATG4A. Inhibition of autophagy by increasing miR-24-3p could be the basis of a strategy to prevent and treat SCLC with combination chemotherapy, particularly in chemoresistant disease."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.2787"xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Song H."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Xu Y."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Wang R."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/author"Pan B."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/name"Oncotarget"xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/pages"317-331"xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/title"Mir-24-3p downregulation contributes to VP16-DDP resistance in small-cell lung cancer by targeting ATG4A."xsd:string
http://purl.uniprot.org/citations/25426560http://purl.uniprot.org/core/volume"6"xsd:string
http://purl.uniprot.org/citations/25426560http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25426560
http://purl.uniprot.org/citations/25426560http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25426560
http://purl.uniprot.org/uniprot/#_B4DEA4-mappedCitation-25426560http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25426560
http://purl.uniprot.org/uniprot/#_G5E979-mappedCitation-25426560http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25426560
http://purl.uniprot.org/uniprot/#_Q8WYN0-mappedCitation-25426560http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25426560
http://purl.uniprot.org/uniprot/Q8WYN0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25426560
http://purl.uniprot.org/uniprot/B4DEA4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25426560
http://purl.uniprot.org/uniprot/G5E979http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25426560