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Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression
Tumor‐associated macrophage (TAM) infiltration facilitates glioma malignancy, but the underlying mechanisms remain unclear. Herein, it is reported that TAMs secrete exosomal LINC01232 to induce tumor immune escape. Mechanistically, LINC01232 is found to directly bind E2F2 and promote E2F2 entry into...
Autores principales: | , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10265094/ https://www.ncbi.nlm.nih.gov/pubmed/37097629 http://dx.doi.org/10.1002/advs.202207067 |
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author | Li, Junjun Wang, Keshan Yang, Chao Zhu, Kai Jiang, Cheng Wang, Minjie Zhou, Zijie Tang, Nan Wang, Qiangping Wang, Siqi Shu, Pengwei Yuan, Hongliang Xiong, Zhiyong Li, Jinsong Liang, Tao Rao, Jin Wang, Xuan Jiang, Xiaobing |
author_facet | Li, Junjun Wang, Keshan Yang, Chao Zhu, Kai Jiang, Cheng Wang, Minjie Zhou, Zijie Tang, Nan Wang, Qiangping Wang, Siqi Shu, Pengwei Yuan, Hongliang Xiong, Zhiyong Li, Jinsong Liang, Tao Rao, Jin Wang, Xuan Jiang, Xiaobing |
author_sort | Li, Junjun |
collection | PubMed |
description | Tumor‐associated macrophage (TAM) infiltration facilitates glioma malignancy, but the underlying mechanisms remain unclear. Herein, it is reported that TAMs secrete exosomal LINC01232 to induce tumor immune escape. Mechanistically, LINC01232 is found to directly bind E2F2 and promote E2F2 entry into the nucleus; the two synergistically promots the transcription of NBR1. The increase in binding between NBR1 binding and the ubiquitinating MHC‐I protein through the ubiquitin domain causes an increase in the degradation of MHC‐I in autophagolysosomes and a decrease in the expression of MHC‐I on the surface of tumor cells, which in turn led to tumor cell escape from CD8(+) CTL immune attack. Disruption of E2F2/NBR1/MHC‐I signaling with shRNAs or blockade with the corresponding antibodies largely abolishes the tumor‐supportive effects of LINC01232 and inhibits tumor growth driven by M2‐type macrophages. Importantly, knockdown of LINC01232 enhances the expression of MHC‐I on the surface of tumor cells and improves the response to reinfusion with CD8(+) T cells. This study reveals the existence of critical molecular crosstalk between TAMs and glioma mediates through the LINC01232/E2F2/NBR1/MHC‐I axis to support malignant tumor growth, indicating that targeting this axis may have therapeutic potential. |
format | Online Article Text |
id | pubmed-10265094 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-102650942023-06-15 Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression Li, Junjun Wang, Keshan Yang, Chao Zhu, Kai Jiang, Cheng Wang, Minjie Zhou, Zijie Tang, Nan Wang, Qiangping Wang, Siqi Shu, Pengwei Yuan, Hongliang Xiong, Zhiyong Li, Jinsong Liang, Tao Rao, Jin Wang, Xuan Jiang, Xiaobing Adv Sci (Weinh) Research Articles Tumor‐associated macrophage (TAM) infiltration facilitates glioma malignancy, but the underlying mechanisms remain unclear. Herein, it is reported that TAMs secrete exosomal LINC01232 to induce tumor immune escape. Mechanistically, LINC01232 is found to directly bind E2F2 and promote E2F2 entry into the nucleus; the two synergistically promots the transcription of NBR1. The increase in binding between NBR1 binding and the ubiquitinating MHC‐I protein through the ubiquitin domain causes an increase in the degradation of MHC‐I in autophagolysosomes and a decrease in the expression of MHC‐I on the surface of tumor cells, which in turn led to tumor cell escape from CD8(+) CTL immune attack. Disruption of E2F2/NBR1/MHC‐I signaling with shRNAs or blockade with the corresponding antibodies largely abolishes the tumor‐supportive effects of LINC01232 and inhibits tumor growth driven by M2‐type macrophages. Importantly, knockdown of LINC01232 enhances the expression of MHC‐I on the surface of tumor cells and improves the response to reinfusion with CD8(+) T cells. This study reveals the existence of critical molecular crosstalk between TAMs and glioma mediates through the LINC01232/E2F2/NBR1/MHC‐I axis to support malignant tumor growth, indicating that targeting this axis may have therapeutic potential. John Wiley and Sons Inc. 2023-04-25 /pmc/articles/PMC10265094/ /pubmed/37097629 http://dx.doi.org/10.1002/advs.202207067 Text en © 2023 The Authors. Advanced Science published by Wiley‐VCH GmbH https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Li, Junjun Wang, Keshan Yang, Chao Zhu, Kai Jiang, Cheng Wang, Minjie Zhou, Zijie Tang, Nan Wang, Qiangping Wang, Siqi Shu, Pengwei Yuan, Hongliang Xiong, Zhiyong Li, Jinsong Liang, Tao Rao, Jin Wang, Xuan Jiang, Xiaobing Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title | Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title_full | Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title_fullStr | Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title_full_unstemmed | Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title_short | Tumor‐Associated Macrophage‐Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC‐I Expression |
title_sort | tumor‐associated macrophage‐derived exosomal linc01232 induces the immune escape in glioma by decreasing surface mhc‐i expression |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10265094/ https://www.ncbi.nlm.nih.gov/pubmed/37097629 http://dx.doi.org/10.1002/advs.202207067 |
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