http://purl.uniprot.org/citations/28202053 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/28202053 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundCisplatin (DDP)-based chemotherapy is the common first-line therapy for lung cancer. However, their efficacy is often limited by primary drug resistance and/or acquired drug resistance. The aim of this study was to investigate the function of miRNA-146a (miR-146a) in DDP-resistant non-small cell lung cancer (NSCLC), as well as the underlying mechanisms.MethodsThe effect of overexpression of miR-146a and/or knockdown of cyclin J (CCNJ) in A549/DDP and SPC-A1/DDP cells were investigated as follows. The cellular sensitivity to DDP, cell apoptosis, cell cycle and cell mobility were detected by CCK-8, flow cytometry, hoechst staining and cell invasion/migration assay, respectively. The effects of miR-146a overexpression in NSCLC resistant cells were further analyzed in a nude mouse xenograft model.ResultsOverexpression of miR-146a and/or knockdown of CCNJ significantly increased the sensitivity to DDP in A549/DDP and SPC-A1/DDP cells compared to NC group via arresting cell cycle, enhancing cell apoptosis, inhibiting cell viability and motility in vitro and in vivo. Furthermore, miR-146a could specially degrade the mRNA of CCNJ, as examined by dual luciferase report assay.ConclusionThe study indicates a crucial role of miR-146a in the development of acquired drug resistance to DDP in NSCLC cells. Further understanding of miR-146a mediated crosstalk networks may promote the clinical use of miR-146a analogue in NSCLC therapy."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.org/dc/terms/identifier | "doi:10.1186/s12885-017-3132-9"xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Huang Y."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Jiang W."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Wu G."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Xu Z."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Shi L."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/author | "Ke B."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/name | "BMC Cancer"xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/pages | "138"xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/title | "Up-regulation of miR-146a increases the sensitivity of non-small cell lung cancer to DDP by downregulating cyclin J."xsd:string |
http://purl.uniprot.org/citations/28202053 | http://purl.uniprot.org/core/volume | "17"xsd:string |
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