Long noncoding RNA MACC1-AS1 promotes the sternness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1/2

Xiaojun Wang; XinnianYu; Wei Wei; Yuanhua Liu

首页> 外文期刊>Environmental toxicology >Long noncoding RNA MACC1-AS1 promotes the sternness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1/2

【24h】

Long noncoding RNA MACC1-AS1 promotes the sternness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1/2

机译：长度非致RNA MACC1-AS1通过促进LATS1 / 2的UPF1介导的稳定性，促进非物质细胞肺癌细胞的沉重。

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相关主题

摘要

The roles of long noncoding RNA (IncRNA) MACC1-AS1 have been revealed in various tumors. This work aims to explore the roles of IncRNA MACC1-AS1 in the sternness of nonsmall cell lung cancer (NSCLC) cells and the underlying mechanism. We showed that overexpression of MACC1-AS1 enhanced the sternness of NSCLC cells, which is evident as the increased expression of cancer stem cell transcription factors, ALDH1 activity, and sphere-formation capacity, while knockdown of MACC1-AS1 decreased it. RNA-sequencing analysis revealed that the Hippo pathway was mostly enriched in NSCLC cell with MACC1-AS1 overexpression. Further mRNA and western blot analysis showed that ectopic expression of MACC1-AS1 regulated the expression LATS1/2, the critical regulator of Hippo pathway. Additionally, it was found that MACC1-AS1 interacted with up-frameshift 1 (UPF1) to modulate mRNA decay of LATS1/2. Overexpression of LAST1/2 attenuated the promoting effects of MACC1-AS1 overexpression on the sternness of NSCLC cells. Therefore, our results demonstrate the effects of the novel MACC1-AS1/UPF1/LATS1/2 axis in NSCLC cell sternness.

机译：在各种肿瘤中揭示了长的非分量RNA（IncRNA）MacC1-AS1的作用。这项工作旨在探讨IncRNA MACC1-AS1在非球细胞肺癌（NSCLC）细胞和潜在机制的级别中的作用。我们表明，MACC1-AS1的过度表达增强了NSCLC细胞的损伤，这显然是癌症干细胞转录因子，ALDH1活性和球形形成能力的增加，而MACC1-AS1的敲低下降。 RNA测序分析显示，河马途径大多富含NSCLC细胞，MACC1-AS1过表达。此外，MRNA和Western印迹分析表明，MACC1-AS1的异位表达调节了河马肺部临界调节剂的表达LATS1 / 2。另外，发现MACC1-AS1与UP-FRAMESHIFT 1（UPF1）相互作用以调节LATS1 / 2的mRNA衰减。 Last1 / 2的过度表达抑制了MACC1-AS1过表达对NSCLC细胞损伤的促进效果。因此，我们的结果展示了新型MACC1-AS1 / UPF1 / LATS1 / 2轴在NSCLC细胞级别中的影响。

著录项

来源
《Environmental toxicology》 |2020年第10期|998-1006|共9页
作者
Xiaojun Wang; XinnianYu; Wei Wei; Yuanhua Liu;
展开▼
作者单位

Department of Thoracic Surgery Nanjing Medical University Affiliated Cancer Hospital & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research Nanjing Jiangsu China;

Department of Medical Oncology Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University Nanjing Jiangsu China;

Department of General Surgery Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University Nanjing Jiangsu China;

Department of Medical Oncology Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University Nanjing Jiangsu China;

展开▼
收录信息
原文格式 PDF
正文语种 eng
中图分类
关键词
LAST1/2; long noncoding RNA; MACC1-AS1; nonsmall cell lung cancer; sternness; up-frameshift 1;

机译：Last1 / 2;长不用RNA;MACC1-AS1;非球体细胞肺癌;严厉;上架1;

Long noncoding RNA MACC1-AS1 promotes the sternness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1/2

摘要

著录项

相关主题

期刊订阅