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Cancer Treat Res Commun. 2024;39:100800. doi: 10.1016/j.ctarc.2024.100800. Epub 2024 Feb 25.
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Pharmacol Res. 2023 Sep;195:106863. doi: 10.1016/j.phrs.2023.106863. Epub 2023 Jul 20.
3
Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer.敲低 RBM15 抑制宫颈癌的肿瘤进展和 JAK-STAT 信号通路。
BMC Cancer. 2023 Jul 20;23(1):684. doi: 10.1186/s12885-023-11163-z.
4
circRNF13, a novel N-methyladenosine-modified circular RNA, enhances radioresistance in cervical cancer by increasing CXCL1 mRNA stability.环状RNA RNF13是一种新型的N-甲基腺苷修饰的环状RNA,它通过提高CXCL1信使核糖核酸的稳定性来增强宫颈癌的放射抗性。
Cell Death Discov. 2023 Jul 20;9(1):253. doi: 10.1038/s41420-023-01557-0.
5
Crosstalk between m6A and coding/non-coding RNA in cancer and detection methods of m6A modification residues.m6A 与癌症中编码/非编码 RNA 的串扰及其修饰残基的检测方法。
Aging (Albany NY). 2023 Jul 11;15(13):6577-6619. doi: 10.18632/aging.204836.
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LINC00426, a novel mA-regulated long non-coding RNA, induces EMT in cervical cancer by binding to ZEB1.LINC00426,一种新型的 mA 调节长非编码 RNA,通过与 ZEB1 结合诱导宫颈癌中的 EMT。
Cell Signal. 2023 Sep;109:110788. doi: 10.1016/j.cellsig.2023.110788. Epub 2023 Jun 29.
7
RBM15 m A modification-mediated OTUB2 upregulation promotes cervical cancer progression via the AKT/mTOR signaling.RBM15 m 通过调节 OTUB2 的表达促进宫颈癌的进展,其作用机制是通过 AKT/mTOR 信号通路。
Environ Toxicol. 2023 Sep;38(9):2155-2164. doi: 10.1002/tox.23852. Epub 2023 Jun 19.
8
PIWI-interacting RNA-17458 is oncogenic and a potential therapeutic target in cervical cancer.PIWI相互作用RNA-17458具有致癌性,是宫颈癌的一个潜在治疗靶点。
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9
FTO promotes the progression of cervical cancer by regulating the N6-methyladenosine modification of ZEB1 and Myc.FTO 通过调控 ZEB1 和 Myc 的 N6-甲基腺苷修饰促进宫颈癌的进展。
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宫颈癌中磁共振扩散峰度成像的研究进展综述

A comprehensive review of mA research in cervical cancer.

机构信息

Key Laboratory of Environmental Medicine & Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, China.

Department of Public Health, Jiangsu Health Vocational College, Nanjing, 210000, China.

出版信息

Epigenomics. 2024;16(10):753-773. doi: 10.2217/epi-2024-0002. Epub 2024 Apr 19.

DOI:10.2217/epi-2024-0002
PMID:38639713
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11318741/
Abstract

Cervical cancer (CC) remains one of the most common malignancies among women worldwide, posing a serious threat to women's health. N6-methyladenosine (mA) modification, as the most abundant type of RNA methylation modification, and has been found to play a crucial role in various cancers. Current research suggests a close association between RNA mA modification and the occurrence and progression of CC, encompassing disruptions in mA levels and its regulatory machinery. This review summarizes the current status of mA modification research in CC, explores the mechanisms underlying mA levels and regulators (methyltransferases, demethylases, reader proteins) in CC and examines the application of small-molecule inhibitors of mA regulators in disease treatment. The findings provide new insights into the future treatment of CC.

摘要

宫颈癌(CC)仍然是全球女性中最常见的恶性肿瘤之一,严重威胁着女性的健康。N6-甲基腺苷(mA)修饰作为最丰富的 RNA 甲基化修饰类型之一,已被发现在各种癌症中发挥关键作用。目前的研究表明,RNA mA 修饰与 CC 的发生和进展密切相关,包括 mA 水平及其调控机制的破坏。本综述总结了 mA 修饰在 CC 中的研究现状,探讨了 CC 中 mA 水平及其调控因子(甲基转移酶、去甲基酶、读码蛋白)的机制,并研究了 mA 调控因子的小分子抑制剂在疾病治疗中的应用。这些发现为 CC 的未来治疗提供了新的思路。