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Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis

Noncoding RNAs (ncRNAs) play important roles in cancer biology, providing potential targets for cancer intervention. As a new class of endogenous noncoding RNAs, circular RNAs (circRNAs) have been recently identified in cell development and function, and certain types of pathological responses contr...

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Autores principales: Yang, Xuanyong, Liu, Yue, Zhou, Xinhui, Chen, Kang, Xu, Jiang, Xu, Shan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Neoplasia Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9468456/
https://www.ncbi.nlm.nih.gov/pubmed/36087384
http://dx.doi.org/10.1016/j.tranon.2022.101515
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author Yang, Xuanyong
Liu, Yue
Zhou, Xinhui
Chen, Kang
Xu, Jiang
Xu, Shan
author_facet Yang, Xuanyong
Liu, Yue
Zhou, Xinhui
Chen, Kang
Xu, Jiang
Xu, Shan
author_sort Yang, Xuanyong
collection PubMed
description Noncoding RNAs (ncRNAs) play important roles in cancer biology, providing potential targets for cancer intervention. As a new class of endogenous noncoding RNAs, circular RNAs (circRNAs) have been recently identified in cell development and function, and certain types of pathological responses contribute to cancer progression, including glioblastoma. However, the potential mechanisms underlying the relationship between circRNAs and glioblastoma progression are still largely unknown. Methods: The expression and roles of circular RNA 0010117 (circ-0010117) were examined in vitro and in vivo. Quantitative RT‒PCR and western blotting were used to measure the expression of circRNA, miRNA, each gene, or related proteins. Cell biology experiments were performed to detect the biological function of circ-0010117 in glioblastoma cell lines. Moreover, bioinformatics analysis, luciferase reporter assays, and functional complementation analysis were carried out to investigate the target genes. Tumorigenesis was also evaluated by xenografting cells into nude mice. In this study, we found that circ-0010117 is downregulated in glioblastoma compared with corresponding paratumoural tissues. Subsequently, we observed that circ-0010117 can regulate aggressiveness in glioblastoma cells through miR-6779-5p. Furthermore, SPEN was verified as a direct target of miR-6779-5p and contributes to the circ-0010117 regulatory network. In addition, we identified that overexpression of circ-0010117 can suppress tumorigenesis in nude mice. Our findings indicate that circular RNA 0010117 promotes the aggressive behavior of glioblastoma by regulating the miRNA-6779-5p/SPEN axis. Our results provide a rationale for the use of circ-0010117 as a novel potential therapeutic target in glioblastoma.
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spelling pubmed-94684562022-09-22 Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis Yang, Xuanyong Liu, Yue Zhou, Xinhui Chen, Kang Xu, Jiang Xu, Shan Transl Oncol Commentary Noncoding RNAs (ncRNAs) play important roles in cancer biology, providing potential targets for cancer intervention. As a new class of endogenous noncoding RNAs, circular RNAs (circRNAs) have been recently identified in cell development and function, and certain types of pathological responses contribute to cancer progression, including glioblastoma. However, the potential mechanisms underlying the relationship between circRNAs and glioblastoma progression are still largely unknown. Methods: The expression and roles of circular RNA 0010117 (circ-0010117) were examined in vitro and in vivo. Quantitative RT‒PCR and western blotting were used to measure the expression of circRNA, miRNA, each gene, or related proteins. Cell biology experiments were performed to detect the biological function of circ-0010117 in glioblastoma cell lines. Moreover, bioinformatics analysis, luciferase reporter assays, and functional complementation analysis were carried out to investigate the target genes. Tumorigenesis was also evaluated by xenografting cells into nude mice. In this study, we found that circ-0010117 is downregulated in glioblastoma compared with corresponding paratumoural tissues. Subsequently, we observed that circ-0010117 can regulate aggressiveness in glioblastoma cells through miR-6779-5p. Furthermore, SPEN was verified as a direct target of miR-6779-5p and contributes to the circ-0010117 regulatory network. In addition, we identified that overexpression of circ-0010117 can suppress tumorigenesis in nude mice. Our findings indicate that circular RNA 0010117 promotes the aggressive behavior of glioblastoma by regulating the miRNA-6779-5p/SPEN axis. Our results provide a rationale for the use of circ-0010117 as a novel potential therapeutic target in glioblastoma. Neoplasia Press 2022-09-07 /pmc/articles/PMC9468456/ /pubmed/36087384 http://dx.doi.org/10.1016/j.tranon.2022.101515 Text en © 2022 Published by Elsevier Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Commentary
Yang, Xuanyong
Liu, Yue
Zhou, Xinhui
Chen, Kang
Xu, Jiang
Xu, Shan
Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title_full Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title_fullStr Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title_full_unstemmed Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title_short Circular RNA 0010117 promotes aggressive glioblastoma behavior by regulating the miRNA-6779-5p/SPEN axis
title_sort circular rna 0010117 promotes aggressive glioblastoma behavior by regulating the mirna-6779-5p/spen axis
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9468456/
https://www.ncbi.nlm.nih.gov/pubmed/36087384
http://dx.doi.org/10.1016/j.tranon.2022.101515
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