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Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12

Tumor-associated exosomes play essential roles in intercellular communication and the foundation of cancer microenvironment in glioma. Many mRNAs, microRNAs (miRNAs) and proteins contained in tumor-associated exosomes can be transferred to recipient cells and contribute to the progression of tumor....

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Autores principales: Bao, Zixu, Zhang, Ning, Niu, Wanxiang, Mu, Maolin, Zhang, Xiaoming, Hu, Shanshan, Niu, Chaoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9391432/
https://www.ncbi.nlm.nih.gov/pubmed/35986010
http://dx.doi.org/10.1038/s41419-022-05097-w
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author Bao, Zixu
Zhang, Ning
Niu, Wanxiang
Mu, Maolin
Zhang, Xiaoming
Hu, Shanshan
Niu, Chaoshi
author_facet Bao, Zixu
Zhang, Ning
Niu, Wanxiang
Mu, Maolin
Zhang, Xiaoming
Hu, Shanshan
Niu, Chaoshi
author_sort Bao, Zixu
collection PubMed
description Tumor-associated exosomes play essential roles in intercellular communication and the foundation of cancer microenvironment in glioma. Many mRNAs, microRNAs (miRNAs) and proteins contained in tumor-associated exosomes can be transferred to recipient cells and contribute to the progression of tumor. Nevertheless, the cellular communication between malignant cells with different heterogeneities or characteristics and resultant tumor progression are still unclear in glioma. Here, we show that exosomes released from glioma stem-like cells (GSCs) contain a significant increasing level of miR-155-5p and could be horizontally transferred to surrounding glioma cells. High expression of miR-155-5p in plasma exosomes from patients was associated with glioma diagnosis and grading. Mechanically, we found that miR-155-5p markedly reduced the expression of acetyl-CoA thioesterase 12 (ACOT12), which played as a tumor suppressor in glioma. Furthermore, mesenchymal transition was significantly promoted in glioma cells treated with GSCs-derived exosomes. In conclusion, GSCs-derived exosomal miR-155-5p play a critical role in glioma progression and facilitating tumor aggressive growth by targeting ACOT12 and promoting mesenchymal transition. Exosomal miR-155-5p is also a potential predictive biomarker for glioma, which may provoke the development of novel diagnostic and therapeutic strategies against glioma.
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spelling pubmed-93914322022-08-21 Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12 Bao, Zixu Zhang, Ning Niu, Wanxiang Mu, Maolin Zhang, Xiaoming Hu, Shanshan Niu, Chaoshi Cell Death Dis Article Tumor-associated exosomes play essential roles in intercellular communication and the foundation of cancer microenvironment in glioma. Many mRNAs, microRNAs (miRNAs) and proteins contained in tumor-associated exosomes can be transferred to recipient cells and contribute to the progression of tumor. Nevertheless, the cellular communication between malignant cells with different heterogeneities or characteristics and resultant tumor progression are still unclear in glioma. Here, we show that exosomes released from glioma stem-like cells (GSCs) contain a significant increasing level of miR-155-5p and could be horizontally transferred to surrounding glioma cells. High expression of miR-155-5p in plasma exosomes from patients was associated with glioma diagnosis and grading. Mechanically, we found that miR-155-5p markedly reduced the expression of acetyl-CoA thioesterase 12 (ACOT12), which played as a tumor suppressor in glioma. Furthermore, mesenchymal transition was significantly promoted in glioma cells treated with GSCs-derived exosomes. In conclusion, GSCs-derived exosomal miR-155-5p play a critical role in glioma progression and facilitating tumor aggressive growth by targeting ACOT12 and promoting mesenchymal transition. Exosomal miR-155-5p is also a potential predictive biomarker for glioma, which may provoke the development of novel diagnostic and therapeutic strategies against glioma. Nature Publishing Group UK 2022-08-19 /pmc/articles/PMC9391432/ /pubmed/35986010 http://dx.doi.org/10.1038/s41419-022-05097-w Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Bao, Zixu
Zhang, Ning
Niu, Wanxiang
Mu, Maolin
Zhang, Xiaoming
Hu, Shanshan
Niu, Chaoshi
Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title_full Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title_fullStr Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title_full_unstemmed Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title_short Exosomal miR-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting ACOT12
title_sort exosomal mir-155-5p derived from glioma stem-like cells promotes mesenchymal transition via targeting acot12
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9391432/
https://www.ncbi.nlm.nih.gov/pubmed/35986010
http://dx.doi.org/10.1038/s41419-022-05097-w
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