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长链非编码RNA核旁斑组装转录本1通过miR-590-3p/MDM2轴促进食管鳞状细胞癌的进展和血管生成。

Long Noncoding RNA Nuclear Paraspeckle Assembly Transcript 1 Promotes Progression and Angiogenesis of Esophageal Squamous Cell Carcinoma Through miR-590-3p/MDM2 Axis.

作者信息

Luo Jing, Xie Kai, Gao Xiang, Yao Yu, Wang Gaoming, Shao Chenye, Li Xiaokun, Xu Yang, Ren Binhui, Hu Liwen, Shen Yi

机构信息

Department of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing, China.

Department of Cardiothoracic Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.

出版信息

Front Oncol. 2021 Feb 19;10:618930. doi: 10.3389/fonc.2020.618930. eCollection 2020.

DOI:10.3389/fonc.2020.618930
PMID:33680941
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7933463/
Abstract

Angiogenesis has been identified as one of the hallmarks of cancer and aggravates cancer development and progression. Accumulating evidence indicated that long noncoding RNAs (lncRNAs) are powerful factors in regulating various cancer behaviors. The aim of this study is to verify the function and potential mechanisms of lncRNA NEAT1 in progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). We found that NEAT1 was overexpressed in ESCC tissues and correlated with clinical characteristics of patients. Silence of NEAT1 inhibited proliferation, migration, invasion and angiogenesis of ESCC cells. High throughput sequencing and western blotting revealed that NEAT1 regulated MDM2/p53 pathway. Rescue of MDM2 restored the effect of NEAT1 on progression and angiogenesis of ESCC cells. Nude mice xenograft models further validated the role of NEAT1 . Importantly, NEAT1 functioned as a competing endogenous RNA for miR-590-3p to regulate MDM2 expression and miR-590-3p acted as a tumor suppressor in ESCC progression and angiogenesis. These findings suggested that NEAT1/miR-590-3p/MDM2 axis might serve as potential therapeutic targets for ESCC patients.

摘要

血管生成已被确定为癌症的标志之一，会加剧癌症的发展和进程。越来越多的证据表明，长链非编码RNA（lncRNA）是调节各种癌症行为的重要因素。本研究的目的是验证lncRNA NEAT1在食管鳞状细胞癌（ESCC）进展和血管生成中的功能及潜在机制。我们发现NEAT1在ESCC组织中过表达，且与患者的临床特征相关。沉默NEAT1可抑制ESCC细胞的增殖、迁移、侵袭和血管生成。高通量测序和蛋白质印迹分析表明，NEAT1调节MDM2/p53通路。恢复MDM2的表达可恢复NEAT1对ESCC细胞进展和血管生成的影响。裸鼠异种移植模型进一步验证了NEAT1的作用。重要的是，NEAT1作为miR-590-3p的竞争性内源性RNA来调节MDM2的表达，而miR-590-3p在ESCC进展和血管生成中起肿瘤抑制作用。这些发现表明，NEAT1/miR-590-3p/MDM2轴可能是ESCC患者潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/0ed8bdfb4007/fonc-10-618930-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/88c4443bbd1f/fonc-10-618930-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/b8dbaa8c49e9/fonc-10-618930-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/0ed8bdfb4007/fonc-10-618930-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/88c4443bbd1f/fonc-10-618930-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/388142ed3d3d/fonc-10-618930-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/f22d4eff5fb4/fonc-10-618930-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/617e/7933463/0ed8bdfb4007/fonc-10-618930-g007.jpg

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