lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2
Lung cancer (LC) is a prevailing primary tumor in the lung. lncRNA non-coding RNA activated by DNA damage (NORAD) is a popular target in human cancers. This experiment is designed to probe the mechanism of lncRNA in LC progression. NORAD expression in normal lung epithelial cells and LC cells was ex...
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Format: | Article |
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De Gruyter
2022-09-01
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Series: | Open Medicine |
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Online Access: | https://doi.org/10.1515/med-2022-0538 |
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author | Mao Wenjun Wang Shengfei Chen Ruo He Yijun Lu Rongguo Zheng Mingfeng |
author_facet | Mao Wenjun Wang Shengfei Chen Ruo He Yijun Lu Rongguo Zheng Mingfeng |
author_sort | Mao Wenjun |
collection | DOAJ |
description | Lung cancer (LC) is a prevailing primary tumor in the lung. lncRNA non-coding RNA activated by DNA damage (NORAD) is a popular target in human cancers. This experiment is designed to probe the mechanism of lncRNA in LC progression. NORAD expression in normal lung epithelial cells and LC cells was examined and then silenced to assess its effect on LC cell proliferation, invasion, and migration. Subcellular localization of NORAD was analyzed through online databases and then corroborated by fractionation of nuclear and cytoplasmic RNA assay. The target binding relations between NORAD and miR-28-3p and between miR-28-3p and E2F2 were verified. Eventually, LC cells with NORAD silencing were transfected with miR-28-3p inhibitor or pcDNA3.1-E2F2 to measure LC cell proliferation, invasion, and migration. NORAD was overexpressed in LC cells and NORAD knockout led to suppressed LC cell proliferation, invasion, and migration. Besides, NORAD targeted miR-28-3p and miR-28-3p targeted E2F2 transcription. Inhibiting miR-28-3p or overexpressing E2F2 could both annul the inhibitory role of si-NORAD in LC cell proliferation, invasion, and migration. Generally, our findings demonstrated that NORAD competitively bound to miR-28-3p with E2F2, to promote LC cell progression. |
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language | English |
last_indexed | 2024-04-10T17:22:44Z |
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spelling | doaj.art-6e047699152546ee9dcc16613e3357052023-02-05T08:27:17ZengDe GruyterOpen Medicine2391-54632022-09-011711538154910.1515/med-2022-0538lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2Mao Wenjun0Wang Shengfei1Chen Ruo2He Yijun3Lu Rongguo4Zheng Mingfeng5Department of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, Jiangsu, ChinaDepartment of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, Jiangsu, ChinaDepartment of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, Jiangsu, ChinaDepartment of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, Jiangsu, ChinaDepartment of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, Jiangsu, ChinaDepartment of Cardiothoracic Surgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, No. 299 Qingyang Road, Wuxi, 214023, Jiangsu, ChinaLung cancer (LC) is a prevailing primary tumor in the lung. lncRNA non-coding RNA activated by DNA damage (NORAD) is a popular target in human cancers. This experiment is designed to probe the mechanism of lncRNA in LC progression. NORAD expression in normal lung epithelial cells and LC cells was examined and then silenced to assess its effect on LC cell proliferation, invasion, and migration. Subcellular localization of NORAD was analyzed through online databases and then corroborated by fractionation of nuclear and cytoplasmic RNA assay. The target binding relations between NORAD and miR-28-3p and between miR-28-3p and E2F2 were verified. Eventually, LC cells with NORAD silencing were transfected with miR-28-3p inhibitor or pcDNA3.1-E2F2 to measure LC cell proliferation, invasion, and migration. NORAD was overexpressed in LC cells and NORAD knockout led to suppressed LC cell proliferation, invasion, and migration. Besides, NORAD targeted miR-28-3p and miR-28-3p targeted E2F2 transcription. Inhibiting miR-28-3p or overexpressing E2F2 could both annul the inhibitory role of si-NORAD in LC cell proliferation, invasion, and migration. Generally, our findings demonstrated that NORAD competitively bound to miR-28-3p with E2F2, to promote LC cell progression.https://doi.org/10.1515/med-2022-0538lung cancerlncrna noradmir-28-3pe2f2competitive endogenous rna cell proliferation |
spellingShingle | Mao Wenjun Wang Shengfei Chen Ruo He Yijun Lu Rongguo Zheng Mingfeng lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 Open Medicine lung cancer lncrna norad mir-28-3p e2f2 competitive endogenous rna cell proliferation |
title | lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 |
title_full | lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 |
title_fullStr | lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 |
title_full_unstemmed | lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 |
title_short | lncRNA NORAD promotes lung cancer progression by competitively binding to miR-28-3p with E2F2 |
title_sort | lncrna norad promotes lung cancer progression by competitively binding to mir 28 3p with e2f2 |
topic | lung cancer lncrna norad mir-28-3p e2f2 competitive endogenous rna cell proliferation |
url | https://doi.org/10.1515/med-2022-0538 |
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