mA 修饰在编码和非编码 RNA 中的作用及其在癌症中的治疗意义。
mA Modification in Coding and Non-coding RNAs: Roles and Therapeutic Implications in Cancer.
机构信息
Department of Systems Biology & the Gehr Family Center for Leukemia Research, the Beckman Research Institute of City of Hope, Monrovia, CA 91016, USA; Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Department of Systems Biology & the Gehr Family Center for Leukemia Research, the Beckman Research Institute of City of Hope, Monrovia, CA 91016, USA; Guangzhou Regenerative Medicine and Health Guangdong Laboratory (GRMH-GDL), Guangzhou 510005, China.
出版信息
Cancer Cell. 2020 Mar 16;37(3):270-288. doi: 10.1016/j.ccell.2020.02.004.
Abstract
N-Methyladenosine (mA) RNA modification has emerged in recent years as a new layer of regulatory mechanism controlling gene expression in eukaryotes. As a reversible epigenetic modification found not only in messenger RNAs but also in non-coding RNAs, mA affects the fate of the modified RNA molecules and plays important roles in almost all vital bioprocesses, including cancer development. Here we review the up-to-date knowledge of the pathological roles and underlying molecular mechanism of mA modifications (in both coding and non-coding RNAs) in cancer pathogenesis and drug response/resistance, and discuss the therapeutic potential of targeting mA regulators for cancer therapy.
摘要
N6-甲基腺苷（m6A）RNA 修饰作为一种新的调控机制，近年来在真核生物中控制基因表达方面备受关注。m6A 是一种可逆的表观遗传修饰，不仅存在于信使 RNA 中，也存在于非编码 RNA 中，它影响修饰 RNA 分子的命运，并在几乎所有重要的生物过程中发挥重要作用，包括癌症的发展。本文综述了 m6A 修饰（在编码和非编码 RNA 中）在癌症发病机制和药物反应/耐药性中的病理作用和潜在分子机制的最新知识，并讨论了针对 m6A 调节剂治疗癌症的治疗潜力。
相似文献
1
mA Modification in Coding and Non-coding RNAs: Roles and Therapeutic Implications in Cancer.mA 修饰在编码和非编码 RNA 中的作用及其在癌症中的治疗意义。
Cancer Cell. 2020 Mar 16;37(3):270-288. doi: 10.1016/j.ccell.2020.02.004.
2
Interaction between N-methyladenosine (mA) modification and noncoding RNAs in cancer.N6-甲基腺苷（m6A）修饰与癌症中非编码 RNA 的相互作用。
Mol Cancer. 2020 May 22;19(1):94. doi: 10.1186/s12943-020-01207-4.
3
Novel insights into the interplay between mA modification and noncoding RNAs in cancer.新型视角解析 mA 修饰与癌症中非编码 RNA 的相互作用。
Mol Cancer. 2020 Aug 7;19(1):121. doi: 10.1186/s12943-020-01233-2.
4
N6-methyladenosine RNA modifications: a potential therapeutic target for AML.N6-甲基腺苷 RNA 修饰：急性髓系白血病的潜在治疗靶点。
Ann Hematol. 2024 Aug;103(8):2601-2612. doi: 10.1007/s00277-023-05302-6. Epub 2023 Aug 7.
5
Comprehensive analyses of m6A regulators and interactive coding and non-coding RNAs across 32 cancer types.对32种癌症类型中的m6A调控因子以及相互作用的编码和非编码RNA进行综合分析。
Mol Cancer. 2021 Apr 13;20(1):67. doi: 10.1186/s12943-021-01362-2.
6
N-methyladenosine methylome in messenger RNA and non-coding RNA.mRNA 和非编码 RNA 中的 N6-甲基腺苷甲基组。
Curr Opin Chem Biol. 2018 Aug;45:179-186. doi: 10.1016/j.cbpa.2018.06.017. Epub 2018 Jul 9.
7
N6-methyladenosine RNA modification and its interaction with regulatory non-coding RNAs in colorectal cancer.N6-甲基腺苷 RNA 修饰及其与结直肠癌中调控性非编码 RNA 的相互作用。
RNA Biol. 2021 Nov 12;18(sup2):551-561. doi: 10.1080/15476286.2021.1974749. Epub 2021 Oct 21.
8
Novel Insights Into the Role of N6-Methyladenosine RNA Modification in Bone Pathophysiology.N6-甲基腺苷 RNA 修饰在骨病理生理学中的作用的新见解。
Stem Cells Dev. 2021 Jan 1;30(1):17-28. doi: 10.1089/scd.2020.0157. Epub 2020 Dec 21.
9
Surmounting cancer drug resistance: New insights from the perspective of N-methyladenosine RNA modification.克服癌症药物耐药性：N6-甲基腺苷 RNA 修饰视角的新见解。
Drug Resist Updat. 2020 Dec;53:100720. doi: 10.1016/j.drup.2020.100720. Epub 2020 Aug 20.
10
N-Methyladenosine in Cancer Immunotherapy: An Undervalued Therapeutic Target.N6-甲基腺苷在癌症免疫治疗中的作用：一个被低估的治疗靶点。
Front Immunol. 2021 Aug 30;12:697026. doi: 10.3389/fimmu.2021.697026. eCollection 2021.
引用本文的文献
1
mA and cardiac posttranscriptional regulation: a novel player in heart development and disease.微小RNA与心脏转录后调控：心脏发育和疾病中的新角色
Exp Mol Med. 2025 Sep 1. doi: 10.1038/s12276-025-01528-8.
2
ALKBH5 in development: decoding the multifaceted roles of mA demethylation in biological processes.发育过程中的ALKBH5：解码m⁶A去甲基化在生物过程中的多方面作用。
Front Mol Biosci. 2025 Aug 4;12:1599487. doi: 10.3389/fmolb.2025.1599487. eCollection 2025.
3
Activated MAFB in ovarian cancer promotes cytoskeletal remodeling and immune microenvironment suppression by interfering with m6A modifications through WTAP competition.卵巢癌中激活的MAFB通过与WTAP竞争干扰m6A修饰，促进细胞骨架重塑和免疫微环境抑制。
Oncogene. 2025 Aug 12. doi: 10.1038/s41388-025-03522-w.
4
m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).非编码RNA的m6A修饰：机制、功能及在人类疾病中的潜在价值（综述）
Int J Mol Med. 2025 Oct;56(4). doi: 10.3892/ijmm.2025.5605. Epub 2025 Aug 8.
5
Epitranscriptomic alterations induced by environmental toxins: implications for RNA modifications and disease.环境毒素诱导的表观转录组改变：对RNA修饰和疾病的影响。
Genes Environ. 2025 Aug 4;47(1):14. doi: 10.1186/s41021-025-00337-9.
6
ALKBH1 drives tumorigenesis and drug resistance via tRNA decoding reprogramming and codon-biased translation.ALKBH1通过tRNA解码重编程和密码子偏向性翻译驱动肿瘤发生和耐药性。
Cancer Discov. 2025 Aug 4. doi: 10.1158/2159-8290.CD-24-1043.
7
M6A RNA modification: focusing on non-small cell lung cancer progression, therapeutic strategies and challenges.m6A RNA修饰：聚焦于非小细胞肺癌的进展、治疗策略及挑战
Front Oncol. 2025 Jul 16;15:1622359. doi: 10.3389/fonc.2025.1622359. eCollection 2025.
8
RNA mA modification: a key regulator in normal and malignant processes.RNA mA修饰：正常和恶性过程中的关键调节因子。
Cell Investig. 2025 Jun;1(2). doi: 10.1016/j.clnves.2025.100023. Epub 2025 Jun 6.
9
The splicing factor SRSF6 mediates ferroptosis resistance in head and neck squamous cell carcinoma through induction of stearoyl-CoA desaturase.剪接因子SRSF6通过诱导硬脂酰辅酶A去饱和酶介导头颈部鳞状细胞癌的铁死亡抗性。
J Biol Chem. 2025 Jul 23;301(9):110509. doi: 10.1016/j.jbc.2025.110509.
10
LncRNA TMEM99 Complexes with IGF2BP2 to Inhibit Autophagy in Lung Adenocarcinoma.长链非编码RNA TMEM99与IGF2BP2形成复合物以抑制肺腺癌中的自噬。
Adv Sci (Weinh). 2025 Sep;12(33):e07871. doi: 10.1002/advs.202507871. Epub 2025 Jul 24.
本文引用的文献
1
DDX3 modulates cisplatin resistance in OSCC through ALKBH5-mediated mA-demethylation of FOXM1 and NANOG.DDX3 通过 ALKBH5 介导的 FOXM1 和 NANOG 的 mA 去甲基化调节 OSCC 中的顺铂耐药性。
Apoptosis. 2020 Apr;25(3-4):233-246. doi: 10.1007/s10495-020-01591-8.
2
-methyladenosine of chromosome-associated regulatory RNA regulates chromatin state and transcription.染色体相关调控 RNA 的 m6A 修饰调控染色质状态和转录。
Science. 2020 Jan 31;367(6477):580-586. doi: 10.1126/science.aay6018. Epub 2020 Jan 16.
3
Oncogenic Role of an Epigenetic Reader of mA RNA Modification: YTHDF1 in Merkel Cell Carcinoma.m⁶A RNA修饰的表观遗传阅读器的致癌作用：YTHDF1在默克尔细胞癌中的作用
Cancers (Basel). 2020 Jan 14;12(1):202. doi: 10.3390/cancers12010202.
4
M6A-mediated upregulation of LINC00958 increases lipogenesis and acts as a nanotherapeutic target in hepatocellular carcinoma.M6A 介导的 LINC00958 上调促进脂肪生成，并作为肝细胞癌的一种纳米治疗靶点。
J Hematol Oncol. 2020 Jan 8;13(1):5. doi: 10.1186/s13045-019-0839-x.
5
mA demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling.mA 去甲基化酶 ALKBH5 通过降低 WIF-1 RNA 甲基化并介导 Wnt 信号通路抑制胰腺癌发生。
Mol Cancer. 2020 Jan 6;19(1):3. doi: 10.1186/s12943-019-1128-6.
6
mA mRNA methylation regulates CTNNB1 to promote the proliferation of hepatoblastoma.mA mRNA 甲基化调控 CTNNB1 促进肝母细胞瘤的增殖。
Mol Cancer. 2019 Dec 23;18(1):188. doi: 10.1186/s12943-019-1119-7.
7
KIAA1429 contributes to liver cancer progression through N6-methyladenosine-dependent post-transcriptional modification of GATA3.KIAA1429 通过 GATA3 的 N6-甲基腺苷依赖性转录后修饰促进肝癌进展。
Mol Cancer. 2019 Dec 19;18(1):186. doi: 10.1186/s12943-019-1106-z.
8
RETRACTED: METTL14 Suppresses CRC Progression via Regulating N6-Methyladenosine-Dependent Primary miR-375 Processing.撤回：METTL14通过调控N6-甲基腺苷依赖的初级miR-375加工来抑制结直肠癌进展。
Mol Ther. 2020 Feb 5;28(2):599-612. doi: 10.1016/j.ymthe.2019.11.016. Epub 2019 Nov 20.
9
The mA eraser FTO facilitates proliferation and migration of human cervical cancer cells.mA 橡皮擦 FTO 促进人宫颈癌细胞的增殖和迁移。
Cancer Cell Int. 2019 Dec 2;19:321. doi: 10.1186/s12935-019-1045-1. eCollection 2019.
10
mA mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-YAP axis to induce NSCLC drug resistance and metastasis.METTL3 介导的 mA mRNA 甲基化直接促进 YAP 翻译，并通过调节 MALAT1-miR-1914-3p-YAP 轴增加 YAP 活性，从而诱导 NSCLC 耐药和转移。
J Hematol Oncol. 2019 Dec 9;12(1):135. doi: 10.1186/s13045-019-0830-6.
Zotero 插件