写入器、读取器和擦除器 RNA 修饰和癌症耐药性。
Writers, readers, and erasers RNA modifications and drug resistance in cancer.
发表日期:2024 Aug 30
作者:
Di Chen, Xinyu Gu, Yeltai Nurzat, Lixia Xu, Xueyuan Li, Lixin Wu, Henan Jiao, Peng Gao, Xuqiang Zhu, Dongming Yan, Shaohua Li, Chen Xue
来源:
CLINICAL PHARMACOLOGY & THERAPEUTICS
摘要:
癌细胞的耐药性显着降低治疗效果,导致复发和转移。造成这种耐药性的一个关键因素是通过 RNA 修饰导致基因表达的表观遗传改变,例如 N6-甲基腺苷 (m6A)、N1-甲基腺苷 (m1A)、5-甲基胞嘧啶 (m5C)、7-甲基鸟苷 (m7G)、假尿苷 (m7G)。 Ψ) 和腺苷到肌苷 (A-to-I) 编辑。这些修饰对于调节 RNA 剪接、翻译、运输、降解和稳定性至关重要。在“写入者”、“读取者”和“擦除者”的控制下,RNA 修饰影响许多生物过程和癌症进展,包括细胞增殖、干性、自噬、侵袭和凋亡。异常的 RNA 修饰可能导致多种癌症的耐药性和不良后果。因此,靶向RNA修饰调节因子为克服耐药性和提高治疗效果提供了一种有前景的策略。这篇综述整合了关于常见 RNA 修饰在癌症耐药性中的作用的最新研究,重点是 m6A、m1A、m5C、m7G、Ψ 和 A-to-I 编辑。此外,它还研究了与癌症耐药性相关的 RNA 修饰的调节机制,并强调了该领域现有的局限性。© 2024。作者。
Drug resistance in cancer cells significantly diminishes treatment efficacy, leading to recurrence and metastasis. A critical factor contributing to this resistance is the epigenetic alteration of gene expression via RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I) editing. These modifications are pivotal in regulating RNA splicing, translation, transport, degradation, and stability. Governed by "writers," "readers," and "erasers," RNA modifications impact numerous biological processes and cancer progression, including cell proliferation, stemness, autophagy, invasion, and apoptosis. Aberrant RNA modifications can lead to drug resistance and adverse outcomes in various cancers. Thus, targeting RNA modification regulators offers a promising strategy for overcoming drug resistance and enhancing treatment efficacy. This review consolidates recent research on the role of prevalent RNA modifications in cancer drug resistance, with a focus on m6A, m1A, m5C, m7G, Ψ, and A-to-I editing. Additionally, it examines the regulatory mechanisms of RNA modifications linked to drug resistance in cancer and underscores the existing limitations in this field.© 2024. The Author(s).