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HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4
BACKGROUND: Vestibular schwannoma (VS) is a kind of benign tumor deriving from the acoustic nerve sheath. Substantial long non-coding RNAs (lncRNAs) were illustrated to have crucial roles in multiple cancers. However, few lncRNAs were elucidated in VS. METHODS: HCG11, miR-620 and ELK4 expression wer...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7786942/ https://www.ncbi.nlm.nih.gov/pubmed/33402177 http://dx.doi.org/10.1186/s12935-020-01691-0 |
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author | Long, Ruiqing Liu, Zhuohui Li, Jinghui Zhang, Yuan Yu, Hualin |
author_facet | Long, Ruiqing Liu, Zhuohui Li, Jinghui Zhang, Yuan Yu, Hualin |
author_sort | Long, Ruiqing |
collection | PubMed |
description | BACKGROUND: Vestibular schwannoma (VS) is a kind of benign tumor deriving from the acoustic nerve sheath. Substantial long non-coding RNAs (lncRNAs) were illustrated to have crucial roles in multiple cancers. However, few lncRNAs were elucidated in VS. METHODS: HCG11, miR-620 and ELK4 expression were tested by RT-qPCR. Gain-of-function experiments were conducted to confirm the effect of HCG11 on VS. RESULTS: HCG11 possessed a low expression in VS cell lines. Overexpression of HCG11 repressed cell proliferation but accelerated apoptosis of VS cells. Moreover, we identified ELK4 stimulated the transcription of HCG11 and their affinity was verified by ChIP assays. MiR-620 was chosen to be a target of HCG11 and it was tested to have a high expression in VS cell lines. Moreover, depletion of miR-620 could inhibit cell proliferative ability while fostering apoptosis rate of VS cells. ELK4 was low expressed in VS cell lines and knockdown of ELK4 could rescue the effects made by HCG11 overexpression on progression of VS. CONCLUSIONS: HCG11 could inhibit the growth of VS by targeting miR-620/ELK4 in VS cells. HCG11 was a novel therapeutic target for VS treatment. |
format | Online Article Text |
id | pubmed-7786942 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-77869422021-01-07 HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 Long, Ruiqing Liu, Zhuohui Li, Jinghui Zhang, Yuan Yu, Hualin Cancer Cell Int Primary Research BACKGROUND: Vestibular schwannoma (VS) is a kind of benign tumor deriving from the acoustic nerve sheath. Substantial long non-coding RNAs (lncRNAs) were illustrated to have crucial roles in multiple cancers. However, few lncRNAs were elucidated in VS. METHODS: HCG11, miR-620 and ELK4 expression were tested by RT-qPCR. Gain-of-function experiments were conducted to confirm the effect of HCG11 on VS. RESULTS: HCG11 possessed a low expression in VS cell lines. Overexpression of HCG11 repressed cell proliferation but accelerated apoptosis of VS cells. Moreover, we identified ELK4 stimulated the transcription of HCG11 and their affinity was verified by ChIP assays. MiR-620 was chosen to be a target of HCG11 and it was tested to have a high expression in VS cell lines. Moreover, depletion of miR-620 could inhibit cell proliferative ability while fostering apoptosis rate of VS cells. ELK4 was low expressed in VS cell lines and knockdown of ELK4 could rescue the effects made by HCG11 overexpression on progression of VS. CONCLUSIONS: HCG11 could inhibit the growth of VS by targeting miR-620/ELK4 in VS cells. HCG11 was a novel therapeutic target for VS treatment. BioMed Central 2021-01-05 /pmc/articles/PMC7786942/ /pubmed/33402177 http://dx.doi.org/10.1186/s12935-020-01691-0 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Primary Research Long, Ruiqing Liu, Zhuohui Li, Jinghui Zhang, Yuan Yu, Hualin HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title | HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title_full | HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title_fullStr | HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title_full_unstemmed | HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title_short | HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4 |
title_sort | hcg11 up-regulation induced by elk4 suppressed proliferation in vestibular schwannoma by targeting mir-620/elk4 |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7786942/ https://www.ncbi.nlm.nih.gov/pubmed/33402177 http://dx.doi.org/10.1186/s12935-020-01691-0 |
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