作者: Lin Shi , Zhaozhong Xu , Gang Wu , Xiaoting Chen , Yuanyuan Huang
DOI: 10.1186/S12885-017-3132-9
关键词: Cyclin 、 Flow cytometry 、 Cell cycle 、 Cisplatin 、 Cancer research 、 Gene knockdown 、 Pathology 、 Medicine 、 Nude mouse 、 Viability assay 、 Apoptosis
摘要: Cisplatin (DDP)-based chemotherapy is the common first-line therapy for lung cancer. However, their efficacy often limited by primary drug resistance and/or acquired resistance. The aim of this study was to investigate function miRNA-146a (miR-146a) in DDP-resistant non-small cell cancer (NSCLC), as well underlying mechanisms. effect overexpression miR-146a knockdown cyclin J (CCNJ) A549/DDP and SPC-A1/DDP cells were investigated follows. cellular sensitivity DDP, apoptosis, cycle mobility detected CCK-8, flow cytometry, hoechst staining invasion/migration assay, respectively. effects NSCLC resistant further analyzed a nude mouse xenograft model. Overexpression CCNJ significantly increased DDP compared NC group via arresting cycle, enhancing inhibiting viability motility vitro vivo. Furthermore, could specially degrade mRNA CCNJ, examined dual luciferase report assay. indicates crucial role development cells. Further understanding mediated crosstalk networks may promote clinical use analogue therapy.