| http://purl.uniprot.org/citations/24582749 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24582749 | http://www.w3.org/2000/01/rdf-schema#comment | "Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) such as gefitinib are clinically effective treatments for non-small cell lung cancer (NSCLC) patients with EGFR activating mutations. However, therapeutic effect is ultimately limited by the development of acquired TKI resistance. MicroRNAs (miRNAs) represent a category of small non-coding RNAs commonly deregulated in human malignancies. The aim of this study was to investigate the role of miRNAs in gefitinib resistance. We established a gefitinib-resistant cell model (PC9GR) by continually exposing PC9 NSCLC cells to gefitinib for 6 months. MiRNA microarray screening revealed miR-138-5p showed the greatest downregulation in PC9GR cells. Re-expression of miR-138-5p was sufficient to sensitize PC9GR cells and another gefitinib-resistant NSCLC cell line, H1975, to gefitinib. Bioinformatics analysis and luciferase reporter assay showed that G protein-coupled receptor124 (GPR124) was a direct target of miR-138-5p. Experimental validation demonstrated that expression of GPR124 was suppressed by miR-138-5p on protein and mRNA levels in NSCLC cells. Furthermore, we observed an inverse correlation between the expression of miR-138-5p and GPR124 in lung adenocarcinoma specimens. Knockdown of GPR124 mimicked the effects of miR-138-5p on the sensitivity to gefitinib. Collectively, our results suggest that downregulation of miR-138-5p contributes to gefitinib resistance and that restoration of miR-138-5p or inhibition GPR124 might serve as potential therapeutic approach for overcoming NSCLC gefitinib resistance."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2014.02.073"xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Deng Y."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Gao Y."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Fan X."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Li W."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Fu X."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/author | "Ping W."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/pages | "179-186"xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/title | "miR-138-5p reverses gefitinib resistance in non-small cell lung cancer cells via negatively regulating G protein-coupled receptor 124."xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://purl.uniprot.org/core/volume | "446"xsd:string |
| http://purl.uniprot.org/citations/24582749 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24582749 |
| http://purl.uniprot.org/citations/24582749 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24582749 |
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