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lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients

BACKGROUND: Non-small cell lung cancer (NSCLC) is a prevalent type of lung cancer worldwide. Long noncoding RNA (lncRNA) SLC9A3-AS1 is reported to play a carcinogenic role in nasopharyngeal carcinoma, but its full-scale role in NSCLC remains elusive. METHODS: SLC9A3-AS1 expression was detected in se...

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Autores principales: Huang, Xiuming, Huang, Mingfang, Chen, Minbiao, Chen, Xianshan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8921674/
https://www.ncbi.nlm.nih.gov/pubmed/35300063
http://dx.doi.org/10.2147/CMAR.S352308
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author Huang, Xiuming
Huang, Mingfang
Chen, Minbiao
Chen, Xianshan
author_facet Huang, Xiuming
Huang, Mingfang
Chen, Minbiao
Chen, Xianshan
author_sort Huang, Xiuming
collection PubMed
description BACKGROUND: Non-small cell lung cancer (NSCLC) is a prevalent type of lung cancer worldwide. Long noncoding RNA (lncRNA) SLC9A3-AS1 is reported to play a carcinogenic role in nasopharyngeal carcinoma, but its full-scale role in NSCLC remains elusive. METHODS: SLC9A3-AS1 expression was detected in serum and tissue of NSLCC patients and NSCLC cell lines. The effects of SLC9A3-AS1 on NSCLC proliferation, migration and invasion were evaluated using CCK-8 and transwell assays. In addition, the potential downstream molecules of SLC9A3-AS1 were searched and explored by bioinformatics analysis, RT-qPCR, dual-luciferase reporter, and rescue experiments. RESULTS: SLC9A3-AS1 was upregulated in NSCLC tissues and cell lines. SLC9A3-AS1 possessed a favorable ability in diagnosing NSCLC. A high level of SLC9A3-AS1 was associated with poor prognosis in NSCLC patients. Functionally, SLC9A3-AS1 knockdown inhibited cell proliferation, migration, and invasion of NSCLC cells. Mechanistically, SLC9A3-AS1 acted as competing endogenous RNA for miR-760 to regulate NSCLC progression. In addition, rescue assay showed that downregulation of miR-760 could reverse the modulatory activity of SLC9A3-AS1 knockdown on NSCLC cells. CONCLUSION: SLC9A3-AS1 was upregulated in NSCLC, and SLC9A3-AS1 knockdown hindered NSCLC progression through targeting miR-760, suggesting that it may prove to be a novel biomarker and therapeutic target for NSCLC.
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spelling pubmed-89216742022-03-16 lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients Huang, Xiuming Huang, Mingfang Chen, Minbiao Chen, Xianshan Cancer Manag Res Original Research BACKGROUND: Non-small cell lung cancer (NSCLC) is a prevalent type of lung cancer worldwide. Long noncoding RNA (lncRNA) SLC9A3-AS1 is reported to play a carcinogenic role in nasopharyngeal carcinoma, but its full-scale role in NSCLC remains elusive. METHODS: SLC9A3-AS1 expression was detected in serum and tissue of NSLCC patients and NSCLC cell lines. The effects of SLC9A3-AS1 on NSCLC proliferation, migration and invasion were evaluated using CCK-8 and transwell assays. In addition, the potential downstream molecules of SLC9A3-AS1 were searched and explored by bioinformatics analysis, RT-qPCR, dual-luciferase reporter, and rescue experiments. RESULTS: SLC9A3-AS1 was upregulated in NSCLC tissues and cell lines. SLC9A3-AS1 possessed a favorable ability in diagnosing NSCLC. A high level of SLC9A3-AS1 was associated with poor prognosis in NSCLC patients. Functionally, SLC9A3-AS1 knockdown inhibited cell proliferation, migration, and invasion of NSCLC cells. Mechanistically, SLC9A3-AS1 acted as competing endogenous RNA for miR-760 to regulate NSCLC progression. In addition, rescue assay showed that downregulation of miR-760 could reverse the modulatory activity of SLC9A3-AS1 knockdown on NSCLC cells. CONCLUSION: SLC9A3-AS1 was upregulated in NSCLC, and SLC9A3-AS1 knockdown hindered NSCLC progression through targeting miR-760, suggesting that it may prove to be a novel biomarker and therapeutic target for NSCLC. Dove 2022-03-09 /pmc/articles/PMC8921674/ /pubmed/35300063 http://dx.doi.org/10.2147/CMAR.S352308 Text en © 2022 Huang et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Huang, Xiuming
Huang, Mingfang
Chen, Minbiao
Chen, Xianshan
lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title_full lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title_fullStr lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title_full_unstemmed lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title_short lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients
title_sort lncrna slc9a3-as1 promotes oncogenesis of nsclc via sponging microrna-760 and may serve as a prognosis predictor of nsclc patients
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8921674/
https://www.ncbi.nlm.nih.gov/pubmed/35300063
http://dx.doi.org/10.2147/CMAR.S352308
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