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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Main Authors: Wen Huang, Xinxing Wang, Fubing Wu, Fanggui Xu
Format: Article
Language:English
Published: BMC 2021-09-01
Series:BMC Pulmonary Medicine
Subjects:
Online Access:https://doi.org/10.1186/s12890-021-01657-6
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spelling 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
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