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Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17

INTRODUCTION: Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of act...

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Autores principales: Wu, Xing-Cheng, Yan, Wei-Gang, Ji, Zhi-Gang, Zheng, Guo-Yang, Liu, Guang-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8641522/
https://www.ncbi.nlm.nih.gov/pubmed/34900057
http://dx.doi.org/10.5114/aoms.2019.85653
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author Wu, Xing-Cheng
Yan, Wei-Gang
Ji, Zhi-Gang
Zheng, Guo-Yang
Liu, Guang-Hua
author_facet Wu, Xing-Cheng
Yan, Wei-Gang
Ji, Zhi-Gang
Zheng, Guo-Yang
Liu, Guang-Hua
author_sort Wu, Xing-Cheng
collection PubMed
description INTRODUCTION: Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of action of SNHG20 in prostate cancer (PCa) are still unclear. MATERIAL AND METHODS: The expression of SNHG20 in PCa tissues and cell lines was detected by RT-qPCR. The correlations between SNHG20 expression and clinicopathological features were analyzed by χ(2) test. The roles of SNHG20 in PCa cell proliferation and migration were detected by CCK-8, EdU incorporation, and transwell assays. The regulatory mechanisms of SNHG20 on DDX17 were detected by dual luciferase reporter assay, RT-qPCR, and western blot. RESULTS: SNHG20 is highly expressed in PCa tissues and cell lines. High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa. CONCLUSIONS: These data showed that SNHG20 promotes PCa cell proliferation and migration via acting as a ceRNA to upregulate DDX17. This study also suggested that SNHG20 may be a potential novel therapeutic target for PCa.
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spelling pubmed-86415222021-12-09 Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17 Wu, Xing-Cheng Yan, Wei-Gang Ji, Zhi-Gang Zheng, Guo-Yang Liu, Guang-Hua Arch Med Sci Basic Research INTRODUCTION: Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of action of SNHG20 in prostate cancer (PCa) are still unclear. MATERIAL AND METHODS: The expression of SNHG20 in PCa tissues and cell lines was detected by RT-qPCR. The correlations between SNHG20 expression and clinicopathological features were analyzed by χ(2) test. The roles of SNHG20 in PCa cell proliferation and migration were detected by CCK-8, EdU incorporation, and transwell assays. The regulatory mechanisms of SNHG20 on DDX17 were detected by dual luciferase reporter assay, RT-qPCR, and western blot. RESULTS: SNHG20 is highly expressed in PCa tissues and cell lines. High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa. CONCLUSIONS: These data showed that SNHG20 promotes PCa cell proliferation and migration via acting as a ceRNA to upregulate DDX17. This study also suggested that SNHG20 may be a potential novel therapeutic target for PCa. Termedia Publishing House 2019-06-06 /pmc/articles/PMC8641522/ /pubmed/34900057 http://dx.doi.org/10.5114/aoms.2019.85653 Text en Copyright: © 2019 Termedia & Banach https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Basic Research
Wu, Xing-Cheng
Yan, Wei-Gang
Ji, Zhi-Gang
Zheng, Guo-Yang
Liu, Guang-Hua
Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title_full Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title_fullStr Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title_full_unstemmed Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title_short Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17
title_sort long noncoding rna snhg20 promotes prostate cancer progression via upregulating ddx17
topic Basic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8641522/
https://www.ncbi.nlm.nih.gov/pubmed/34900057
http://dx.doi.org/10.5114/aoms.2019.85653
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