http://purl.uniprot.org/citations/27582507 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/27582507 | http://www.w3.org/2000/01/rdf-schema#comment | "Acquisition of drug-resistant phenotypes is often associated with chemotherapy in osteosarcoma. A number of studies have demonstrated a critical role for autophagy in osteosarcoma development, therapy and drug resistance. However, the molecular mechanisms underlying the autophagy-mediated chemotherapy resistance of osteosarcoma cells remain largely unknown. In the present study, we determined the autophagy and microRNA-140 (miR-140-5p, miRBase ID: MIMAT0000431) expression induced by chemotherapeutic drugs in osteosarcoma cells. Then we determined the promotory role of miR-140-5p to the chemotherapy-induced autophagy. Our results demonstrated that miR-140-5p expression was highly induced during chemotherapy of osteosarcoma cells, and this was accompanied by up-regulated autophagy. The increased miR-140-5p expression levels up-regulated anticancer drug-induced autophagy in osteosarcoma cells and ameliorated the anticancer drug-induced cell proliferation and viability decrease. Importantly, miR-140-5p regulates this context-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (IP3k2). Therefore, the results of the present study demonstrated that miR-140-5p mediated drug-resistance in osteosarcoma cells by inducing autophagy. The present study provides evidence of miRNA regulation of autophagy through modulation of IP3 signalling. The present study recognized a novel mechanism of chemoresistance in osteosarcoma cancers."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.org/dc/terms/identifier | "doi:10.1042/bsr20160238"xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/author | "Deng Z."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/author | "Cai L."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/author | "Su J."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/author | "Wei R."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/author | "Cao G."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/name | "Biosci Rep"xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/pages | "e00392"xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/title | "miR-140-5p attenuates chemotherapeutic drug-induced cell death by regulating autophagy through inositol 1,4,5-trisphosphate kinase 2 (IP3k2) in human osteosarcoma cells."xsd:string |
http://purl.uniprot.org/citations/27582507 | http://purl.uniprot.org/core/volume | "36"xsd:string |
http://purl.uniprot.org/citations/27582507 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/27582507 |
http://purl.uniprot.org/citations/27582507 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/27582507 |
http://purl.uniprot.org/uniprot/#_B2R9J0-mappedCitation-27582507 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27582507 |
http://purl.uniprot.org/uniprot/#_P27987-mappedCitation-27582507 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/27582507 |
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http://purl.uniprot.org/uniprot/P27987 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/27582507 |
http://purl.uniprot.org/uniprot/Q2TU82 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/27582507 |
http://purl.uniprot.org/uniprot/B2R9J0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/27582507 |