...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biochemical Genetics >Long Non-coding RNA MIAT Mediates Non-small Cell Lung Cancer Development Through Regulating the miR-128-3p/PELI3 Axis
【24h】

Long Non-coding RNA MIAT Mediates Non-small Cell Lung Cancer Development Through Regulating the miR-128-3p/PELI3 Axis

机译：长期非编码RNA MIAT通过调节MIR-128-3P / PELI3轴介导非小细胞肺癌发育

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

In this study, we set out to characterize the expression status of long non-coding RNA (lncRNA) Myocardial Infarction Associated Transcript (MIAT) in non-small cell lung cancer (NSCLC) and elucidate its mechanistic contribution to this disease. Relative expression levels of MIAT, Pellino E3 Ubiquitin Protein Ligase Family Member 3 (PELI3), and microRNA (miR)-128-3p were analyzed by real-time polymerase chain reaction. PELI3 protein level was determined by immunoblotting. Cell viability and proliferation were evaluated by the MTT assay and colony formation assay, respectively. Cell invasion and migration were assessed by wound-healing closure and transwell assays, respectively. The regulatory actions of miR-128-3p on both MIAT and PELI3 were interrogated by luciferase reporter assay. We demonstrated the aberrant upregulation of MIAT in NSCLC and its association with tumor progression. We further uncovered the negative correlation among MIAT, PELI3, and miR-128-3p. MIAT deficiency significantly compromised cell viability, proliferation, invasion, and migration, while increased miR-128-3p and decreased PELI3 expressions. Application of miR-128-3p inhibitor significantly stimulated luciferase activities driven by both MIAT and PELI3 promoter and phenotypically promoted cell viability, proliferation, migration, and invasion. Our study highlighted the mechanistic contribution of the MIAT/miR-128-3p/PELI3 signaling cascade in NSCLC.
机译：在这项研究中，我们开始表征非小细胞肺癌（NSCLC）中长的非编码RNA（LNCRNA）心肌梗死相关转录物（MIAI）的表达状态，并阐明其对该疾病的机械贡献。采用实时聚合酶链反应分析了MIAI，髓核E3泛素蛋白连接酶3（PELI3）和MICRRNA（MIR）-128-3P的相对表达水平。通过免疫印迹测定peli3蛋白质水平。通过MTT测定和菌落形成测定法评估细胞活力和增殖。通过伤口愈合闭合和翻转测定分别评估细胞侵袭和迁移。通过荧光素酶报告器测定询问MIR-128-3P对MIAI和PELI3的调节作用。我们证明了NSCLC中的MIAT的异常上调及其与肿瘤进展的关系。我们进一步揭示了MIAT，PELI3和MIR-128-3P之间的负相关。 Miat缺乏症明显受损，细胞活力，增殖，侵袭和迁移，同时增加miR-128-3p并降低了Peli3表达。 MiR-128-3P抑制剂的应用显着刺激了MIAI AIAI AIAI AIV和PELI3启动子和表型促进的细胞活力，增殖，迁移和侵袭的荧光素酶活性。我们的研究强调了NSCLC中Miat / MiR-128-3P / PELI3信号传导级联的机械贡献。

著录项

  • 来源
    《Biochemical Genetics》 |2020年第6期|共16页
  • 作者

    Li Fannian; Li Haitao; Li Shuai; Lv Baolei; Shi Junjie; Yan Hongjiang; Zhang Helin; He Yuzheng;

  • 作者单位

    First Hosp Xingtai Dept Thorac Surg 376 Shunde Rd Xingtai 054001 Hebei Peoples R China;

    Hebei Med Univ Hosp 2 Dept Pulm &

    Crit Care Med 215 Heping West Rd Shijiazhuang 050000 Hebei;

    Hebei Med Univ Hosp 2 Dept Pulm &

    Crit Care Med 215 Heping West Rd Shijiazhuang 050000 Hebei;

    First Hosp Shijiazhuang Dept Thorac Surg 36 Fanxi Rd Shijiazhuang 050011 Hebei Peoples R China;

    Handan First Hosp Dept Thorac Surg 25 Congtai Rd Handan 056002 Peoples R China;

    Hebei Med Univ Hosp 2 Dept Thorac Surg 215 Heping West Rd Shijiazhuang 050000 Hebei Peoples R;

    Hebei Med Univ Hosp 2 Dept Thorac Surg 215 Heping West Rd Shijiazhuang 050000 Hebei Peoples R;

    Hebei Med Univ Hosp 2 Dept Thorac Surg 215 Heping West Rd Shijiazhuang 050000 Hebei Peoples R;

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

    Non-small-cell lung cancer; MIAT; miR-128-3p; PELI3;

    机译：非小细胞肺癌;miat;mir-128-3p;peli3;

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