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RNA 甲基化在癌症进展、自噬和抗癌药物耐药性中的作用。

Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance.

机构信息

Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea.

出版信息

Int J Mol Sci. 2023 Feb 20;24(4):4225. doi: 10.3390/ijms24044225.

DOI:10.3390/ijms24044225
PMID:36835633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9959100/
Abstract

RNA methylations play critical roles in RNA processes, including RNA splicing, nuclear export, nonsense-mediated RNA decay, and translation. Regulators of RNA methylations have been shown to be differentially expressed between tumor tissues/cancer cells and adjacent tissues/normal cells. N6-methyladenosine (m6A) is the most prevalent internal modification of RNAs in eukaryotes. m6A regulators include m6A writers, m6A demethylases, and m6A binding proteins. Since m6A regulators play important roles in regulating the expression of oncogenes and tumor suppressor genes, targeting m6A regulators can be a strategy for developing anticancer drugs. Anticancer drugs targeting m6A regulators are in clinical trials. m6A regulator-targeting drugs could enhance the anticancer effects of current chemotherapy drugs. This review summarizes the roles of m6A regulators in cancer initiation and progression, autophagy, and anticancer drug resistance. The review also discusses the relationship between autophagy and anticancer drug resistance, the effect of high levels of m6A on autophagy and the potential values of m6A regulators as diagnostic markers and anticancer therapeutic targets.

摘要

RNA 甲基化在 RNA 过程中发挥着关键作用,包括 RNA 剪接、核输出、无义介导的 RNA 衰变和翻译。RNA 甲基化调节剂在肿瘤组织/癌细胞和相邻组织/正常细胞之间的表达存在差异。N6-甲基腺苷(m6A)是真核生物中最普遍的 RNA 内部修饰。m6A 调节剂包括 m6A 写入器、m6A 去甲基酶和 m6A 结合蛋白。由于 m6A 调节剂在调节癌基因和肿瘤抑制基因的表达中起着重要作用,因此靶向 m6A 调节剂可以成为开发抗癌药物的一种策略。针对 m6A 调节剂的抗癌药物正在临床试验中。m6A 调节剂靶向药物可以增强现有化疗药物的抗癌效果。本文综述了 m6A 调节剂在癌症发生和进展、自噬以及抗癌药物耐药性中的作用。本文还讨论了自噬与抗癌药物耐药性的关系、高水平 m6A 对自噬的影响以及 m6A 调节剂作为诊断标志物和抗癌治疗靶点的潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/f4cf607d3c81/ijms-24-04225-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/06b7211036aa/ijms-24-04225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/9b6d5600847f/ijms-24-04225-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/f4cf607d3c81/ijms-24-04225-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/06b7211036aa/ijms-24-04225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/9b6d5600847f/ijms-24-04225-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c6/9959100/f4cf607d3c81/ijms-24-04225-g003.jpg

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