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LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis

BACKGROUND: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high mortality worldwide. Long non-coding RNA (lncRNA) TTN antisense RNA1 (TTN-AS1) has been demonstrated to play a crucial role in a variety of cancers. This study was designed to investigate the function and...

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Autores principales: Qi, Guanbin, Li, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335898/
https://www.ncbi.nlm.nih.gov/pubmed/32669856
http://dx.doi.org/10.2147/OTT.S238890
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author Qi, Guanbin
Li, Lei
author_facet Qi, Guanbin
Li, Lei
author_sort Qi, Guanbin
collection PubMed
description BACKGROUND: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high mortality worldwide. Long non-coding RNA (lncRNA) TTN antisense RNA1 (TTN-AS1) has been demonstrated to play a crucial role in a variety of cancers. This study was designed to investigate the function and molecular mechanism of lncRNA TTN-AS1 in NSCLC. METHODS: The expression levels of TTN-AS1, miR-491-5p and zinc finger protein 503 (ZNF503) were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assay, respectively. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell migration and invasion were assessed by transwell assay. Epithelial-to-mesenchymal transition (EMT)-related proteins were measured using Western blot assay. The relationship between TTN-AS1, miR-491-5p and ZNF503 was predicted by starBase2.0 and confirmed by dual-luciferase reporter assay. Xenograft tumor experiment was conducted to analyze the tumor growth in vivo. RESULTS: The levels of TTN-AS1 and ZNF503 were up-regulated, while miR-491-5p expression was reduced in NSCLC tissues and cells. Knockdown of TTN-AS1 or ZNF503 suppressed cell proliferation, migration, invasion and EMT in NSCLC cells. Overexpression of ZNF503 reversed the effect of TTN-AS1 silencing on NSCLC progression. TTN-AS1 could modulate the expression of ZNF503 via sponging miR-491-5p. Furthermore, TTN-AS1 induced tumor growth in vivo. CONCLUSION: Inhibition of TTN-AS1 hindered cell proliferation, migration, invasion and EMT in NSCLC cells by modulating miR-491-5p/ZNF503 axis, providing a promising biomarker for NSCLC treatment.
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spelling pubmed-73358982020-07-14 LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis Qi, Guanbin Li, Lei Onco Targets Ther Original Research BACKGROUND: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high mortality worldwide. Long non-coding RNA (lncRNA) TTN antisense RNA1 (TTN-AS1) has been demonstrated to play a crucial role in a variety of cancers. This study was designed to investigate the function and molecular mechanism of lncRNA TTN-AS1 in NSCLC. METHODS: The expression levels of TTN-AS1, miR-491-5p and zinc finger protein 503 (ZNF503) were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assay, respectively. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell migration and invasion were assessed by transwell assay. Epithelial-to-mesenchymal transition (EMT)-related proteins were measured using Western blot assay. The relationship between TTN-AS1, miR-491-5p and ZNF503 was predicted by starBase2.0 and confirmed by dual-luciferase reporter assay. Xenograft tumor experiment was conducted to analyze the tumor growth in vivo. RESULTS: The levels of TTN-AS1 and ZNF503 were up-regulated, while miR-491-5p expression was reduced in NSCLC tissues and cells. Knockdown of TTN-AS1 or ZNF503 suppressed cell proliferation, migration, invasion and EMT in NSCLC cells. Overexpression of ZNF503 reversed the effect of TTN-AS1 silencing on NSCLC progression. TTN-AS1 could modulate the expression of ZNF503 via sponging miR-491-5p. Furthermore, TTN-AS1 induced tumor growth in vivo. CONCLUSION: Inhibition of TTN-AS1 hindered cell proliferation, migration, invasion and EMT in NSCLC cells by modulating miR-491-5p/ZNF503 axis, providing a promising biomarker for NSCLC treatment. Dove 2020-07-01 /pmc/articles/PMC7335898/ /pubmed/32669856 http://dx.doi.org/10.2147/OTT.S238890 Text en © 2020 Qi and Li. http://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/). 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
Qi, Guanbin
Li, Lei
LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title_full LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title_fullStr LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title_full_unstemmed LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title_short LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis
title_sort lncrna ttn-as1 promotes progression of non-small cell lung cancer via regulating mir-491-5p/znf503 axis
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335898/
https://www.ncbi.nlm.nih.gov/pubmed/32669856
http://dx.doi.org/10.2147/OTT.S238890
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