CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Role of N6-methyladenosine RNA modification in cancer.
Role of N6-methyladenosine RNA modification in cancer.
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N6-甲基腺苷(m6A)是真核细胞中含量最丰富的RNA修饰。既往研究表明,m6A在多种疾病尤其是癌症中发挥关键作用。m6A与癌症的发生、进展、耐药、侵袭和转移相关。
然而,尽管有这些认识,对其在癌症复杂背景下的具体作用和机制仍缺乏全面理解。本综述首先概述m6A修饰的关键调控蛋白及其翻译后修饰(PTMs),以及在癌细胞中染色质可及性和转录活性中的作用。
此外,本文强调m6A修饰通过调控程序性细胞死亡机制以及通过各种癌症相关免疫细胞影响肿瘤微环境来影响癌症进展。进一步,本综述讨论了微生物如何通过改变m6A修饰在微生物相关癌症中诱导持久表观遗传改变和致癌效应。
最后,本文深入探讨m6A修饰在癌症免疫治疗中的作用,包括RNA治疗、免疫检查点阻断、细胞因子治疗、过继细胞转移治疗以及直接靶向m6A调控因子。
总体而言,本综述阐明了m6A修饰在癌症中的多方面作用,并探索了旨在操纵m6A修饰的靶向治疗,以期推动癌症研究并改善患者预后。
N6-methyladenosine (m6A) is the most abundant modification of RNA in eukaryotic cells. Previous studies have shown that m6A is pivotal in diverse diseases especially cancer. m6A corelates with the initiation, progression, resistance, invasion, and metastasis of cancer.
However, despite these insights, a comprehensive understanding of its specific roles and mechanisms within the complex landscape of cancer is still elusive. This review begins by outlining the key regulatory proteins of m6A modification and their posttranslational modifications (PTMs), as well as the role in chromatin accessibility and transcriptional activity within cancer cells.
Additionally, it highlights that m6A modifications impact cancer progression by modulating programmed cell death mechanisms and affecting the tumor microenvironment through various cancer-associated immune cells.
Furthermore, the review discusses how microorganisms can induce enduring epigenetic changes and oncogenic effect in microorganism-associated cancers by altering m6A modifications. Last, it delves into the role of m6A modification in cancer immunotherapy, encompassing RNA therapy, immune checkpoint blockade, cytokine therapy, adoptive cell transfer therapy, and direct targeting of m6A regulators.
Overall, this review clarifies the multifaceted role of m6A modification in cancer and explores targeted therapies aimed at manipulating m6A modification, aiming to advance cancer research and improve patient outcomes.
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