...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Oncology letters >MicroRNA-199a-5p inhibits cisplatin-induced drug resistance via inhibition of autophagy in osteosarcoma cells
【24h】

MicroRNA-199a-5p inhibits cisplatin-induced drug resistance via inhibition of autophagy in osteosarcoma cells

机译：MicroRNA-199a-5p通过抑制骨肉瘤细胞中的自噬来抑制顺铂诱导的耐药性

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Osteosarcoma (OS) is the most common cancer of the bone. Chemotherapy is commonly used for the clinical treatment of OS. However, chemoresistance to cisplatin [also known as diamminedichloridoplatinum (II) (DDP)] is a major obstacle for OS therapy, the underlying mechanism of which is not fully understood. The present study aimed to investigate the role of microRNA (miR)-199a-5p in the regulation of chemoresistance to DDP in OS cells. Reverse transcription-quantitative polymerase chain reaction demonstrated that the expression level of miR-199a-5p was significantly reduced in human OS MG63 cells. In addition, DDP treatment also upregulated the protein levels of light chain 3 (LC3)-II and Beclin1 as well as the ratio of LC3-II vs. LC3-I in MG63 cells, indicating that autophagy was activated. Restoration of miR-199a-5p expression promoted DDP-induced inhibition of MG63 cell proliferation and inhibited DDP-induced autophagy, as indicated by the reduced protein levels of LC3-II and Beclin1 and the ratio of LC3-II vs. LC3-I. Finally, luciferase reporter assay data revealed that miR-199a-5p directly targeted Beclin1 and negatively mediated Beclin1 expression at a post-transcriptional level in MG63 cells. In conclusion, our study suggests that miR-199a-5p promotes the cytotoxicity of DDP in OS cells via inhibition of autophagy. Therefore, miR-199a-5p/autophagy signaling is involved in chemoresistance and may become a potential target for the treatment of DDP-resistant OS.
机译：骨肉瘤（OS）是最常见的骨癌。化学疗法通常用于OS的临床治疗。然而，对顺铂的化学耐药性[也被称为二氨二氯铂（II）（DDP）]是OS治疗的主要障碍，其潜在机制尚不完全清楚。本研究旨在研究microRNA（miR）-199a-5p在调节OS细胞对DDP的化学耐药性中的作用。逆转录定量聚合酶链反应表明，miR-199a-5p的表达水平在人OS MG63细胞中显着降低。此外，DDP处理还上调了MG63细胞中轻链3（LC3）-II和Beclin1的蛋白质水平以及LC3-II与LC3-I的比率，表明自噬被激活。 miR-199a-5p表达的恢复促进了DDP诱导的对MG63细胞增殖的抑制，并抑制了DDP诱导的自噬，如LC3-II和Beclin1蛋白水平降低以及LC3-II与LC3-I的比例降低所表明的。最后，荧光素酶报告基因检测数据表明，miR-199a-5p直接靶向Beclin1，并在MG63细胞中以转录后水平负向介导Beclin1表达。总之，我们的研究表明miR-199a-5p通过抑制自噬促进OS细胞中DDP的细胞毒性。因此，miR-199a-5p /自噬信号传导参与化学耐药性，可能成为治疗DDP耐药OS的潜在靶标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号