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mA 修饰在免疫逃逸和免疫治疗中的作用。

Role of mA modifications in immune evasion and immunotherapy.

机构信息

NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.

Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, China.

出版信息

Med Oncol. 2024 May 18;41(6):159. doi: 10.1007/s12032-024-02402-9.

DOI:10.1007/s12032-024-02402-9
PMID:38761335
Abstract

RNA modification has garnered increasing attention in recent years due to its pivotal role in tumorigenesis and immune surveillance. N-methyladenosine (mA) modification is the most prevalent RNA modification, which can affect the expression of RNA by methylating adenylate at the sixth N position to regulate the occurrence and development of tumors. Dysregulation of mA affects the activation of cancer-promoting pathways, destroys immune cell function, maintains immunosuppressive microenvironment, and promotes tumor cell growth. In this review, we delve into the latest insights into how abnormalities in mA modification in both tumor and immune cells orchestrate immune evasion through the activation of signaling pathways. Furthermore, we explore how dysregulated mA modification in tumor cells influences immune cells, thereby regulating tumor immune evasion via interactions within the tumor microenvironment (TME). Lastly, we highlight recent discoveries regarding specific inhibitors of mA modulators and the encapsulation of mA-targeting nanomaterials for cancer therapy, discussing their potential applications in immunotherapy.

摘要

近年来,RNA 修饰因其在肿瘤发生和免疫监视中的关键作用而受到越来越多的关注。N6-甲基腺苷(m6A)修饰是最普遍的 RNA 修饰之一,它可以通过将腺苷酸的第六位 N 甲基化来调节肿瘤的发生和发展。m6A 的失调会影响 RNA 的表达,从而激活促进癌症的途径,破坏免疫细胞的功能,维持免疫抑制微环境,并促进肿瘤细胞的生长。在这篇综述中,我们深入探讨了肿瘤细胞和免疫细胞中 m6A 修饰的异常如何通过激活信号通路来协调免疫逃逸,以及肿瘤细胞中失调的 m6A 修饰如何通过肿瘤微环境(TME)内的相互作用影响免疫细胞,从而调节肿瘤免疫逃逸。最后,我们重点介绍了最近关于 m6A 修饰调节剂的特异性抑制剂和 m6A 靶向纳米材料在癌症治疗中的封装的发现,讨论了它们在免疫治疗中的潜在应用。

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USP2 promotes tumor immune evasion via deubiquitination and stabilization of PD-L1.USP2 通过去泛素化和稳定 PD-L1 促进肿瘤免疫逃逸。
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Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment.
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ALKBH5 抑制通过促进 Ccl28 m6A 修饰和增加 Treg 募集来减轻雄性小鼠的 I/R 诱导的肾损伤。
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