• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>RSC Advances >miR-199a-3p knockdown inhibits dedifferentiated liposarcoma (DDLPS) cell viability and enhances apoptosis through targeting casein kinase-1 alpha (CK1 alpha)
【24h】

miR-199a-3p knockdown inhibits dedifferentiated liposarcoma (DDLPS) cell viability and enhances apoptosis through targeting casein kinase-1 alpha (CK1 alpha)

机译：miR-199A-3P敲低抑制去脱脂剂（DDLPS）细胞活力并通过靶向酪蛋白激酶-1α（CK1α）增强细胞凋亡

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Dedifferentiated liposarcoma (DDLPS) is an aggressive tumor with high mortality. More insight into the biology of DDLPS tumorigenesis is needed to devise novel therapeutic approaches. Previous data showed that miRNA-199a-3p (miR-199a-3p) was strongly upregulated in DDLPS tissues. However, the biological role of miR-199a-3p in DDLPS remains unknown. In this study, we detected miR-199a-3p expression using RT-qPCR and observed that miR-199a-3p was more highly expressed in DDLPS tissues and cell lines (SW872 and LPS141). Functionally, MTT assay, flow cytometry and western blot results demonstrated that knockdown of miR-199a-3p inhibited DDLPS cell viability, enhanced apoptosis rate, and decreased expression of apoptosis-related genes Bax and cleaved caspase 3, as well as increased Bcl-2 expression in vitro. Moreover, xenograft tumors were generated and miR-199a-3p knockdown could suppress DDLPS xenograft tumor growth accompanying decreased proliferating cell nuclear antigen (PCNA) level and increased cleaved caspase 3 level in vivo. Mechanically, luciferase reporter assay and RNA immunoprecipitation (RIP) identified that CK1 alpha was targeted and downregulated by miR-199a-3p. Expression of CK1 alpha was lower in DDLPS tissues. Besides, there was a negative linear correlation between expressions of miR-199a-3p and CK1 alpha in DDLPS tissues. Rescue experiments indicated that CK1 alpha silencing could abolish the effect of miR-199a-3p knockdown on cell viability and apoptosis in DDLPS cells in vitro. In conclusion, knockdown of miR-199a-3p inhibits DDLPS cell viability and enhances apoptosis through targeting CK1 alpha in vitro and in vivo. Our results suggest miR-199a-3p/CK1 alpha axis may be a novel pathogen of DDLPS.
机译：Deffifferentiated Liposarcoma（DDLPS）是一种高死亡率的激进肿瘤。需要对DDLPS肿瘤发生的生物学的更多洞察力来设计新的治疗方法。以前的数据显示MiRNA-199A-3P（MiR-199A-3P）在DDLPS组织中强烈上调。然而，MIR-199A-3P在DDLPS中的生物学作用仍然未知。在这项研究中，我们使用RT-QPCR检测miR-199A-3P表达，观察到MiR-199A-3P在DDLPS组织和细胞系中更高度表达（SW872和LPS141）。在功能上，MTT测定，流式细胞术和Western印迹结果表明，MiR-199A-3P的敲低抑制了DDLPS细胞活力，增强的凋亡率，并降低了凋亡相关基因的表达和切割的Caspase 3的表达，以及增加的Bcl-2体外表达。此外，生成异种移植肿瘤，MIR-199A-3P敲低可以抑制DDLPS异种移植肿瘤生长随着减少的增殖细胞核抗原（PCNA）水平，并在体内增加了切割的胱天蛋白酶3水平。机械地，荧光素酶报告器测定和RNA免疫沉淀（RIP）确定CK1α靶向和下调MiR-199A-3P。 DDLPS组织中CK1α的表达较低。此外，在DDLPS组织中miR-199A-3P和CK1α的表达式之间存在负线性相关性。救援实验表明，CK1α沉默可以在体外解除MIR-199A-3P敲低对细胞活力和细胞凋亡的影响。总之，MIR-199A-3P的敲低抑制DDLPS细胞活力并通过体外和体内靶向CK1α来增强细胞凋亡。我们的结果表明MiR-199A-3P / CK1α轴可能是DDLP的新病原体。

著录项

  • 来源
    《RSC Advances》 |2019年第39期|共9页
  • 作者

    Cao Ye; Zheng Jiajia; Lv Chentao;

  • 作者单位

    Shanghai Publ Hlth Clin Ctr Dept Gen Surg 921 Rd Tongxin Shanghai 200083 Peoples R China;

    Zhongshan Hosp &

    Red Cross Hosp Dept Gen Surg Shanghai 200030 Peoples R China;

    Shanghai Publ Hlth Clin Ctr Dept Gen Surg 921 Rd Tongxin Shanghai 200083 Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
  • 关键词

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