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SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis
BACKGROUND: Astrocytoma is a common tumor type in primary central nervous system and has a high death rate around the world. Aberrant expression of long non-coding RNAs (lncRNAs) has been introduced by emerging studies to result in the development of diverse cancers. METHODS: RT-qPCR examined the ex...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469335/ https://www.ncbi.nlm.nih.gov/pubmed/32883232 http://dx.doi.org/10.1186/s12885-020-07280-8 |
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author | Du, Fengping Hou, Qian |
author_facet | Du, Fengping Hou, Qian |
author_sort | Du, Fengping |
collection | PubMed |
description | BACKGROUND: Astrocytoma is a common tumor type in primary central nervous system and has a high death rate around the world. Aberrant expression of long non-coding RNAs (lncRNAs) has been introduced by emerging studies to result in the development of diverse cancers. METHODS: RT-qPCR examined the expression of SNHG17, miR-876-5p and ERLIN2, and western blot evaluated ERLIN2 protein level. RNA pull down and luciferase reporter assays illustrated the relationships between SNHG17 and its downstream molecules. RESULTS: SNHG17 was up-regulated in astrocytoma cells. Moreover, SNHG17 silence could repress the proliferation, migration and invasion of astrocytoma cells. Besides, miR-876-5p was selected out as a downstream molecule of SNHG17 in astrocytoma. ERLIN2 was determined to be targeted by miR-876-5p. ERLIN2 mRNA and protein levels were lessened by miR-876-5p overexpression and SNHG17 silence. Additionally, miR-876-5p overexpression decelerated the biological processes of astrocytoma cells, so did ERLIN2 knockdown. More importantly, the impacts of SNHG17 down-regulation on the malignant behaviors of astrocytoma cells were counteracted by overexpressed ERLIN2 or inhibited miR-876-5p. CONCLUSIONS: SNHG17 could induce the progression of astrocytoma by sponging miR-876-5p to elevate the expression of ERLIN2. This study indicated that SNHG17 has a high potential to be a therapeutic target for astrocytoma. |
format | Online Article Text |
id | pubmed-7469335 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-74693352020-09-03 SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis Du, Fengping Hou, Qian BMC Cancer Research Article BACKGROUND: Astrocytoma is a common tumor type in primary central nervous system and has a high death rate around the world. Aberrant expression of long non-coding RNAs (lncRNAs) has been introduced by emerging studies to result in the development of diverse cancers. METHODS: RT-qPCR examined the expression of SNHG17, miR-876-5p and ERLIN2, and western blot evaluated ERLIN2 protein level. RNA pull down and luciferase reporter assays illustrated the relationships between SNHG17 and its downstream molecules. RESULTS: SNHG17 was up-regulated in astrocytoma cells. Moreover, SNHG17 silence could repress the proliferation, migration and invasion of astrocytoma cells. Besides, miR-876-5p was selected out as a downstream molecule of SNHG17 in astrocytoma. ERLIN2 was determined to be targeted by miR-876-5p. ERLIN2 mRNA and protein levels were lessened by miR-876-5p overexpression and SNHG17 silence. Additionally, miR-876-5p overexpression decelerated the biological processes of astrocytoma cells, so did ERLIN2 knockdown. More importantly, the impacts of SNHG17 down-regulation on the malignant behaviors of astrocytoma cells were counteracted by overexpressed ERLIN2 or inhibited miR-876-5p. CONCLUSIONS: SNHG17 could induce the progression of astrocytoma by sponging miR-876-5p to elevate the expression of ERLIN2. This study indicated that SNHG17 has a high potential to be a therapeutic target for astrocytoma. BioMed Central 2020-09-03 /pmc/articles/PMC7469335/ /pubmed/32883232 http://dx.doi.org/10.1186/s12885-020-07280-8 Text en © The Author(s) 2020 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 | Research Article Du, Fengping Hou, Qian SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title | SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title_full | SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title_fullStr | SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title_full_unstemmed | SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title_short | SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis |
title_sort | snhg17 drives malignant behaviors in astrocytoma by targeting mir-876-5p/erlin2 axis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469335/ https://www.ncbi.nlm.nih.gov/pubmed/32883232 http://dx.doi.org/10.1186/s12885-020-07280-8 |
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