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Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p

The antisense transcript of SATB2 protein (SATB2-AS1) is a novel long non-coding RNA (lncRNA) which is involved in the development of colorectal cancer, breast cancer and hepatocellular carcinoma. In the present study, it was aimed to investigate the consequent situation of SATB2-AS1 in tissue and c...

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Autores principales: Gu, Jia, Ye, Yongqing, Sunil, Rauniyar, Zhan, Wenjian, Yu, Rutong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10562957/
https://www.ncbi.nlm.nih.gov/pubmed/37822583
http://dx.doi.org/10.3892/etm.2023.12202
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author Gu, Jia
Ye, Yongqing
Sunil, Rauniyar
Zhan, Wenjian
Yu, Rutong
author_facet Gu, Jia
Ye, Yongqing
Sunil, Rauniyar
Zhan, Wenjian
Yu, Rutong
author_sort Gu, Jia
collection PubMed
description The antisense transcript of SATB2 protein (SATB2-AS1) is a novel long non-coding RNA (lncRNA) which is involved in the development of colorectal cancer, breast cancer and hepatocellular carcinoma. In the present study, it was aimed to investigate the consequent situation of SATB2-AS1 in tissue and cell lines of glioma. The expression of SATB2-AS1 in glioma cases was analyzed in The Cancer Genome Atlas datasets. The glycolytic metabolism was determined in glioma cells by detection of extracellular glucose level, oxygen consumption rate and extracellular acidification rate. Cell Counting Kit-8 assay and flow cytometry were used to assess cell proliferation and apoptosis in glioma cells. The interaction between SATB2-AS1 and microRNA (miR)-671-5p was verified by bioinformatic analysis, reverse transcription-quantitative PCR, dual luciferase reporter assay and RNA immunoprecipitation assay. The expression levels of the downstream targets of SATB2-AS1 were studied by western blotting. Results demonstrated that SATB2-AS1 was a downregulated lncRNA in low grade glioma and glioblastoma. Gain-of-function assay demonstrated that SATB2-AS1 inhibited cell proliferation, and glycolytic metabolism, while induced cell apoptosis in glioma cells. SATB2-AS1 sponged and suppressed the expression of an oncogenic miRNA miR-671-5p. By regulation of miR-671-5p, SATB2-AS1 upregulated cerebellar degeneration related protein 1 (CDR1) and Visinin-like 1 (VSNL1) expression in glioma cells. miR-671-5p overexpression partially reversed the antitumor effect of SATB2-AS1 in glioma. In conclusion, the current study demonstrated that there was a downregulation of SATB2-AS1 in glioma, and SATB2-AS1 regulated miR-671-5p/CDR1 axis and miR-671-5p/VSNL1 axis in glioma.
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spelling pubmed-105629572023-10-11 Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p Gu, Jia Ye, Yongqing Sunil, Rauniyar Zhan, Wenjian Yu, Rutong Exp Ther Med Articles The antisense transcript of SATB2 protein (SATB2-AS1) is a novel long non-coding RNA (lncRNA) which is involved in the development of colorectal cancer, breast cancer and hepatocellular carcinoma. In the present study, it was aimed to investigate the consequent situation of SATB2-AS1 in tissue and cell lines of glioma. The expression of SATB2-AS1 in glioma cases was analyzed in The Cancer Genome Atlas datasets. The glycolytic metabolism was determined in glioma cells by detection of extracellular glucose level, oxygen consumption rate and extracellular acidification rate. Cell Counting Kit-8 assay and flow cytometry were used to assess cell proliferation and apoptosis in glioma cells. The interaction between SATB2-AS1 and microRNA (miR)-671-5p was verified by bioinformatic analysis, reverse transcription-quantitative PCR, dual luciferase reporter assay and RNA immunoprecipitation assay. The expression levels of the downstream targets of SATB2-AS1 were studied by western blotting. Results demonstrated that SATB2-AS1 was a downregulated lncRNA in low grade glioma and glioblastoma. Gain-of-function assay demonstrated that SATB2-AS1 inhibited cell proliferation, and glycolytic metabolism, while induced cell apoptosis in glioma cells. SATB2-AS1 sponged and suppressed the expression of an oncogenic miRNA miR-671-5p. By regulation of miR-671-5p, SATB2-AS1 upregulated cerebellar degeneration related protein 1 (CDR1) and Visinin-like 1 (VSNL1) expression in glioma cells. miR-671-5p overexpression partially reversed the antitumor effect of SATB2-AS1 in glioma. In conclusion, the current study demonstrated that there was a downregulation of SATB2-AS1 in glioma, and SATB2-AS1 regulated miR-671-5p/CDR1 axis and miR-671-5p/VSNL1 axis in glioma. D.A. Spandidos 2023-09-11 /pmc/articles/PMC10562957/ /pubmed/37822583 http://dx.doi.org/10.3892/etm.2023.12202 Text en Copyright: © Gu et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Gu, Jia
Ye, Yongqing
Sunil, Rauniyar
Zhan, Wenjian
Yu, Rutong
Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title_full Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title_fullStr Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title_full_unstemmed Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title_short Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p
title_sort downregulation of lncrna satb2‑as1 facilitates glioma cell proliferation by sponging mir‑671‑5p
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10562957/
https://www.ncbi.nlm.nih.gov/pubmed/37822583
http://dx.doi.org/10.3892/etm.2023.12202
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