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LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319
INTRODUCTION: NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development. METHODS: The PCAT18 expression in NSCLC tissues and cell lin...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8122005/ https://www.ncbi.nlm.nih.gov/pubmed/34007211 http://dx.doi.org/10.2147/CMAR.S298918 |
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author | He, Li Wang, Jianjun Zhou, Long Li, Xiaobing |
author_facet | He, Li Wang, Jianjun Zhou, Long Li, Xiaobing |
author_sort | He, Li |
collection | PubMed |
description | INTRODUCTION: NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development. METHODS: The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319. RESULTS: PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo. CONCLUSION: In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC. |
format | Online Article Text |
id | pubmed-8122005 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-81220052021-05-17 LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 He, Li Wang, Jianjun Zhou, Long Li, Xiaobing Cancer Manag Res Original Research INTRODUCTION: NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development. METHODS: The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319. RESULTS: PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo. CONCLUSION: In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC. Dove 2021-05-10 /pmc/articles/PMC8122005/ /pubmed/34007211 http://dx.doi.org/10.2147/CMAR.S298918 Text en © 2021 He 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 He, Li Wang, Jianjun Zhou, Long Li, Xiaobing LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title | LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title_full | LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title_fullStr | LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title_full_unstemmed | LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title_short | LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319 |
title_sort | lncrna pcat18 promotes non-small cell lung cancer progression by sponging mir-4319 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8122005/ https://www.ncbi.nlm.nih.gov/pubmed/34007211 http://dx.doi.org/10.2147/CMAR.S298918 |
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