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N6-甲基腺苷RNA甲基化,免疫微环境中代谢重编程的一个新标志。

N6-methyladenosine RNA methylation, a new hallmark of metabolic reprogramming in the immune microenvironment.

作者信息

Li Xiaoyue, Peng Lin, Yang Xuelian, Luo Jing, Wang Jianmei, Mou Kelin, Zhou Huan, Luo Yuhao, Xiang Li

机构信息

Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

School of Life Sciences, Yunnan University, Kunming, China.

出版信息

Front Immunol. 2024 Dec 20;15:1464042. doi: 10.3389/fimmu.2024.1464042. eCollection 2024.

DOI:10.3389/fimmu.2024.1464042
PMID:39759516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11695279/
Abstract

N6-methyladenosine is one of the most common and reversible post-transcriptional modifications in eukaryotes, and it is involved in alternative splicing and RNA transcription, degradation, and translation. It is well known that cancer cells acquire energy through metabolic reprogramming to exhibit various biological behaviors. Moreover, numerous studies have demonstrated that m6A induces cancer metabolic reprogramming by regulating the expression of core metabolic genes or by activating metabolic signaling pathways. Meanwhile, m6A modifications and related regulators are key targets in the regulation of immune effects. We further summarize how m6A modifications contribute to tumor metabolism, and how these events affect the tumor immune microenvironment, with a specific focus on different cell types. Finally, we focus on the specific applications of this field to tumor immunotherapy. We review the potential role of m6A in metabolic reprogramming of tumor immune microenvironment and its regulatory mechanism, with the aim of providing new targets for tumor metabolic regulation and immunotherapy.

摘要

N6-甲基腺苷是真核生物中最常见且可逆的转录后修饰之一,它参与可变剪接以及RNA的转录、降解和翻译过程。众所周知,癌细胞通过代谢重编程获取能量以展现出各种生物学行为。此外,大量研究表明,m6A通过调节核心代谢基因的表达或激活代谢信号通路来诱导癌症代谢重编程。同时,m6A修饰及其相关调节因子是免疫效应调节的关键靶点。我们进一步总结了m6A修饰如何促进肿瘤代谢,以及这些事件如何影响肿瘤免疫微环境,特别关注不同的细胞类型。最后,我们聚焦于该领域在肿瘤免疫治疗中的具体应用。我们综述了m6A在肿瘤免疫微环境代谢重编程中的潜在作用及其调控机制,旨在为肿瘤代谢调节和免疫治疗提供新的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/8089556490b0/fimmu-15-1464042-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/25774027de00/fimmu-15-1464042-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/0f2a4a9c61b6/fimmu-15-1464042-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/1ac7c7ed52be/fimmu-15-1464042-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/8089556490b0/fimmu-15-1464042-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/25774027de00/fimmu-15-1464042-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/0f2a4a9c61b6/fimmu-15-1464042-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/1ac7c7ed52be/fimmu-15-1464042-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ec/11695279/8089556490b0/fimmu-15-1464042-g004.jpg

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Metabolic regulation of the glioblastoma stem cell epitranscriptome by malate dehydrogenase 2.通过苹果酸脱氢酶 2 对神经胶质瘤干细胞转录组的代谢调控。
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