肝细胞癌中细胞生存压力与 N6-甲基腺苷修饰之间的串扰。
The crosstalk between cellular survival pressures and N6-methyladenosine modification in hepatocellular carcinoma.
发表日期:2024 Aug 10
作者:
Chu-Li Fu, Zheng-Wei Zhao, Qiang-Nu Zhang
来源:
BIOMEDICINE & PHARMACOTHERAPY
摘要:
在肿瘤微环境中,生存压力普遍存在,是肿瘤进展、血管生成和治疗耐药的有力驱动因素。 N6-甲基腺苷 (m6A) 甲基化已被认为是调节 mRNA 代谢各个方面的关键转录后机制。了解生存压力和 m6A 修饰之间复杂的相互作用,为了解肝细胞癌 (HCC) 进展的分子机制提供了新的见解,并强调了在 HCC 诊断和治疗中针对生存压力-m6A 轴的潜力。 MEDLINE 和 Web of Science 查找截至 2024 年 4 月发表的相关文章。用于搜索的关键词包括肝细胞癌、细胞生存、生存压力、N6-甲基腺苷、肿瘤微环境、应激反应和缺氧。这篇综述深入探讨了多方面的问题生存压力和 m6A RNA 甲基化在 HCC 中的作用,强调生存压力如何调节 m6A 景观、m6A 修饰对生存压力响应基因表达的影响,以及对 HCC 细胞生存、增殖、转移和治疗耐药性的后续影响。此外,我们探索了针对这种串扰的治疗潜力,提出了利用对生存压力和 m6A RNA 甲基化机制的理解来开发新的、更有效的 HCC 治疗方法的策略。生存压力和 m6A RNA 甲基化之间的相互作用表现为一种复杂的相互作用。影响 HCC 发病和进展的调控网络。版权所有 © 2024 浙江大学医学院附属第一医院。由 Elsevier B.V. 出版。保留所有权利。
Within the tumor microenvironment, survival pressures are prevalent with potent drivers of tumor progression, angiogenesis, and therapeutic resistance. N6-methyladenosine (m6A) methylation has been recognized as a critical post-transcriptional mechanism regulating various aspects of mRNA metabolism. Understanding the intricate interplay between survival pressures and m6A modification provides new insights into the molecular mechanisms underlying hepatocellular carcinoma (HCC) progression and highlights the potential for targeting the survival pressures-m6A axis in HCC diagnosis and treatment.A literature search was conducted in PubMed, MEDLINE, and Web of Science for relevant articles published up to April 2024. The keywords used for the search included hepatocellular carcinoma, cellular survival, survival pressure, N6-methyladenosine, tumor microenvironment, stress response, and hypoxia.This review delves into the multifaceted roles of survival pressures and m6A RNA methylation in HCC, highlighting how survival pressures modulate the m6A landscape, the impact of m6A modification on survival pressure-responsive gene expression, and the consequent effects on HCC cell survival, proliferation, metastasis, and resistance to treatment. Furthermore, we explored the therapeutic potential of targeting this crosstalk, proposing strategies that leverage the understanding of survival pressures and m6A RNA methylation mechanisms to develop novel, and more effective treatments for HCC.The interplay between survival pressures and m6A RNA methylation emerges as a complex regulatory network that influences HCC pathogenesis and progression.Copyright © 2024 First Affiliated Hospital, Zhejiang University School of Medicine in China. Published by Elsevier B.V. All rights reserved.