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N6-甲基腺嘌呤修饰对消化道肿瘤代谢重编程的影响。

Effects of N6-methyladenosine modification on metabolic reprogramming in digestive tract tumors.

作者信息

Yu Liang, Gao Yuan, Bao Qiongling, Xu Min, Lu Juan, Du Weibo

机构信息

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.

出版信息

Heliyon. 2024 Jan 11;10(2):e24414. doi: 10.1016/j.heliyon.2024.e24414. eCollection 2024 Jan 30.

DOI:10.1016/j.heliyon.2024.e24414
PMID:38293446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10826742/
Abstract

N6-methyladenosine (m6A), the most abundant RNA modification within cells, participates in various biological and pathological processes, including self-renewal, invasion and proliferation, drug resistance, and stem cell characteristics. The m6A methylation plays a crucial role in tumors by regulating multiple RNA processes such as transcription, processing, and translation. Three protein types are primarily involved in m6A methylation: methyltransferases (such as METTL3, METTL14, ZC3H13, and KIAA1429), demethylases (such as FTO, ALKBH5), and RNA-binding proteins (such as the family of YTHDF, YTHDC1, YTHDC2, and IGF2BPs). Various metabolic pathways are reprogrammed in digestive tumors to meet the heightened growth demands and sustain cellular functionality. Recent studies have highlighted the extensive impact of m6A on the regulation of digestive tract tumor metabolism, further modulating tumor initiation and progression. Our review aims to provide a comprehensive understanding of the expression patterns, functional roles, and regulatory mechanisms of m6A in digestive tract tumor metabolism-related molecules and pathways. The characterization of expression profiles of m6A regulatory factors and in-depth studies on m6A methylation in digestive system tumors may provide new directions for clinical prediction and innovative therapeutic interventions.

摘要

N6-甲基腺嘌呤(m6A)是细胞内最丰富的RNA修饰,参与各种生物学和病理过程,包括自我更新、侵袭和增殖、耐药性以及干细胞特性。m6A甲基化通过调节转录、加工和翻译等多种RNA过程在肿瘤中发挥关键作用。主要有三种蛋白质类型参与m6A甲基化:甲基转移酶(如METTL3、METTL14、ZC3H13和KIAA1429)、去甲基酶(如FTO、ALKBH5)和RNA结合蛋白(如YTHDF家族、YTHDC1、YTHDC2和IGF2BPs)。在消化肿瘤中,各种代谢途径被重新编程,以满足增加的生长需求并维持细胞功能。最近的研究强调了m6A对消化道肿瘤代谢调节的广泛影响,进一步调节肿瘤的发生和进展。我们的综述旨在全面了解m6A在消化道肿瘤代谢相关分子和途径中的表达模式、功能作用及调控机制。m6A调控因子表达谱的特征分析以及对消化系统肿瘤中m6A甲基化的深入研究可能为临床预测和创新治疗干预提供新方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/8ebbc6312948/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/4fd5ba4232f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/6f18adbed771/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/8ebbc6312948/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/4fd5ba4232f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/6f18adbed771/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174b/10826742/8ebbc6312948/gr3.jpg

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2
METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression.METTL16 促进糖酵解代谢重编程和结直肠癌进展。
J Exp Clin Cancer Res. 2023 Jun 20;42(1):151. doi: 10.1186/s13046-023-02732-y.
3
m6A modification on the fate of colorectal cancer: functions and mechanisms of cell proliferation and tumorigenesis.N6-甲基腺嘌呤(m6A)修饰对结直肠癌命运的影响:细胞增殖和肿瘤发生的功能及机制
Front Oncol. 2023 Apr 21;13:1162300. doi: 10.3389/fonc.2023.1162300. eCollection 2023.
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Crosstalk between N6-methyladenosine (m6A) modification and noncoding RNA in tumor microenvironment.m6A 修饰与肿瘤微环境中非编码 RNA 的串扰。
Int J Biol Sci. 2023 Apr 17;19(7):2198-2219. doi: 10.7150/ijbs.79651. eCollection 2023.
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m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1α positive feedback loop.m6A 甲基化通过 ALKBH5-HDAC4-HIF1α 正反馈环调节缺氧诱导的胰腺癌糖酵解代谢。
Oncogene. 2023 Jun;42(25):2047-2060. doi: 10.1038/s41388-023-02704-8. Epub 2023 May 6.
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Purine anabolism creates therapeutic vulnerability in hepatocellular carcinoma through m 6 A-mediated epitranscriptomic regulation.嘌呤合成代谢通过 m6A 介导的表观转录组调控在肝细胞癌中产生治疗脆弱性。
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