LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop
Abstract Background Lung adenocarcinoma (LUAD) is the most common histological subtype of primary lung cancer. To identify the biomarker of diagnosis for LUAD is of great significance. Long non-coding RNAs (lncRNAs) were previously revealed to exert vital effects in numerous cancers. LncRNA long int...
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doaj-372f0558729e4ed0a7ae024cd900e02d2021-09-12T11:49:26ZengBMCBMC Pulmonary Medicine1471-24662021-09-0121111210.1186/s12890-021-01657-6LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loopWen Huang0Xinxing Wang1Fubing Wu2Fanggui Xu3Department of Oncology, The Fourth Affiliated Hospital of Nanjing Medical UniversityDepartment of Oncology, Sir Run Run Hospital of Nanjing Medical UniversityDepartment of Oncology, Sir Run Run Hospital of Nanjing Medical UniversityDepartment of Oncology, Sir Run Run Hospital of Nanjing Medical UniversityAbstract Background Lung adenocarcinoma (LUAD) is the most common histological subtype of primary lung cancer. To identify the biomarker of diagnosis for LUAD is of great significance. Long non-coding RNAs (lncRNAs) were previously revealed to exert vital effects in numerous cancers. LncRNA long intergenic non-protein coding RNA 520 (LINC00520) served as an oncogene in various cancers. Therefore, our study was specially designed to probe the role of LINC00520 in LUAD. Results LINC00520 expression was detected by RT-qPCR. Next, function of LINC00520 in LUAD was verified by in vitro loss-of-function experiments. DNA pull down, ChIP, RIP, and luciferase reporter assays were conducted to reveal the regulatory mechanism of LINC00520. We found that LINC00520 was upregulated in LUAD. Additionally, LINC00520 upregulation is associated with the poor prognosis for patients with LUAD. Furthermore, LINC00520 downregulation suppressed LUAD cell proliferation and migration and induced cell apoptosis. Forkhead box P3 (FOXP3) is identified as the transcription factor to transcriptionally activate LINC00520. Moreover, LINC00520 positively upregulated FOXP3 expression via sponging miR-3611 in LUAD cells. Subsequently, rescue experiments delineated that miR-3611 downregulation or FOXP3 overexpression reversed the effects of silenced LINC00520 on proliferative and migratory capabilities in LUAD cells. Conclusion This study innovatively indicated that lncRNA LINC00520 facilitated cell proliferative and migratory abilities in LUAD through interacting with miR-3611 and targeting FOXP3, which may provide a potential novel insight for treatment of LUAD.https://doi.org/10.1186/s12890-021-01657-6Lung adenocarcinomaLINC00520FOXP3Transcription factormiR-3611 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Wen Huang Xinxing Wang Fubing Wu Fanggui Xu |
spellingShingle |
Wen Huang Xinxing Wang Fubing Wu Fanggui Xu LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop BMC Pulmonary Medicine Lung adenocarcinoma LINC00520 FOXP3 Transcription factor miR-3611 |
author_facet |
Wen Huang Xinxing Wang Fubing Wu Fanggui Xu |
author_sort |
Wen Huang |
title |
LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
title_short |
LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
title_full |
LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
title_fullStr |
LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
title_full_unstemmed |
LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
title_sort |
lncrna linc00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop |
publisher |
BMC |
series |
BMC Pulmonary Medicine |
issn |
1471-2466 |
publishDate |
2021-09-01 |
description |
Abstract Background Lung adenocarcinoma (LUAD) is the most common histological subtype of primary lung cancer. To identify the biomarker of diagnosis for LUAD is of great significance. Long non-coding RNAs (lncRNAs) were previously revealed to exert vital effects in numerous cancers. LncRNA long intergenic non-protein coding RNA 520 (LINC00520) served as an oncogene in various cancers. Therefore, our study was specially designed to probe the role of LINC00520 in LUAD. Results LINC00520 expression was detected by RT-qPCR. Next, function of LINC00520 in LUAD was verified by in vitro loss-of-function experiments. DNA pull down, ChIP, RIP, and luciferase reporter assays were conducted to reveal the regulatory mechanism of LINC00520. We found that LINC00520 was upregulated in LUAD. Additionally, LINC00520 upregulation is associated with the poor prognosis for patients with LUAD. Furthermore, LINC00520 downregulation suppressed LUAD cell proliferation and migration and induced cell apoptosis. Forkhead box P3 (FOXP3) is identified as the transcription factor to transcriptionally activate LINC00520. Moreover, LINC00520 positively upregulated FOXP3 expression via sponging miR-3611 in LUAD cells. Subsequently, rescue experiments delineated that miR-3611 downregulation or FOXP3 overexpression reversed the effects of silenced LINC00520 on proliferative and migratory capabilities in LUAD cells. Conclusion This study innovatively indicated that lncRNA LINC00520 facilitated cell proliferative and migratory abilities in LUAD through interacting with miR-3611 and targeting FOXP3, which may provide a potential novel insight for treatment of LUAD. |
topic |
Lung adenocarcinoma LINC00520 FOXP3 Transcription factor miR-3611 |
url |
https://doi.org/10.1186/s12890-021-01657-6 |
work_keys_str_mv |
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