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N⁶-甲基腺苷(m⁶A)修饰在癌症中的作用:最新进展与未来方向

The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.

作者信息

Xie Xiaozhou, Fang Zhen, Zhang Haoyu, Wang Zheng, Li Jie, Jia Yuchen, Shang Liang, Cao Feng, Li Fei

机构信息

Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.

Department of Gastrointestinal Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

出版信息

EXCLI J. 2025 Jan 15;24:113-150. doi: 10.17179/excli2024-7935. eCollection 2025.

DOI:10.17179/excli2024-7935
PMID:39967906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11830918/
Abstract

N(6)-methyladenosine (m6A) modification is the most abundant and prevalent internal modification in eukaryotic mRNAs. The role of m6A modification in cancer has become a hot research topic in recent years and has been widely explored. m6A modifications have been shown to regulate cancer occurrence and progression by modulating different target molecules. This paper reviews the recent research progress of m6A modifications in cancer and provides an outlook on future research directions, especially the development of molecularly targeted drugs. See also the graphical abstract(Fig. 1).

摘要

N⁶-甲基腺苷(m⁶A)修饰是真核生物mRNA中最丰富且普遍存在的内部修饰。近年来,m⁶A修饰在癌症中的作用已成为热门研究课题,并得到了广泛探索。m⁶A修饰已被证明可通过调节不同的靶分子来调控癌症的发生和发展。本文综述了m⁶A修饰在癌症方面的最新研究进展,并对未来的研究方向,尤其是分子靶向药物的开发进行了展望。另见图1的图形摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/a63044cb685f/EXCLI-24-113-g-003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/531b6e201751/EXCLI-24-113-t-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/d7f04f1faad4/EXCLI-24-113-g-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/e8920b902e9b/EXCLI-24-113-g-002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/a63044cb685f/EXCLI-24-113-g-003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/531b6e201751/EXCLI-24-113-t-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/d7f04f1faad4/EXCLI-24-113-g-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/e8920b902e9b/EXCLI-24-113-g-002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d8f/11830918/a63044cb685f/EXCLI-24-113-g-003.jpg

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本文引用的文献

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Environmental Risk Factors for Gallbladder Cancer: Field-Wide Systematic Review and Meta-Analysis.胆囊癌的环境危险因素:全领域系统评价与荟萃分析
Clin Gastroenterol Hepatol. 2024 Oct 5. doi: 10.1016/j.cgh.2024.07.046.
2
A novel protein SPECC1-415aa encoded by N6-methyladenosine modified circSPECC1 regulates the sensitivity of glioblastoma to TMZ.一种新型蛋白 SPECC1-415aa,由 N6-甲基腺苷修饰的 circSPECC1 编码,可调节胶质母细胞瘤对 TMZ 的敏感性。
Cell Mol Biol Lett. 2024 Sep 27;29(1):127. doi: 10.1186/s11658-024-00644-z.
3
Nod-like receptors: The relevant elements of glioblastoma`s prognostic puzzle.
核苷酸结合寡聚化结构域样受体:胶质母细胞瘤预后谜题的相关要素。
Pharmacol Res. 2024 Oct;208:107411. doi: 10.1016/j.phrs.2024.107411. Epub 2024 Sep 11.
4
METTL3-Mediated mA Modification of FMRP Drives Hepatocellular Carcinoma Progression and Indicates Poor Prognosis.METTL3介导的FMRP的m⁶A修饰驱动肝细胞癌进展并提示预后不良。
Cancer Biother Radiopharm. 2024 Dec;39(10):745-754. doi: 10.1089/cbr.2023.0186. Epub 2024 Sep 12.
5
N-methyladenosine (mA) writer METTL5 represses the ferroptosis and antitumor immunity of gastric cancer.N-甲基腺苷(mA)书写蛋白METTL5抑制胃癌的铁死亡和抗肿瘤免疫。
Cell Death Discov. 2024 Sep 11;10(1):402. doi: 10.1038/s41420-024-02166-1.
6
METTL3 inhibitor suppresses the progression of prostate cancer via IGFBP3/AKT pathway and synergizes with PARP inhibitor.METTL3 抑制剂通过 IGFBP3/AKT 通路抑制前列腺癌的进展,并与 PARP 抑制剂协同作用。
Biomed Pharmacother. 2024 Oct;179:117366. doi: 10.1016/j.biopha.2024.117366. Epub 2024 Sep 3.
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METTL16-SENP3-LTF axis confers ferroptosis resistance and facilitates tumorigenesis in hepatocellular carcinoma.METTL16-SENP3-LTF 轴赋予肝癌细胞对铁死亡的抗性并促进肿瘤发生。
J Hematol Oncol. 2024 Sep 2;17(1):78. doi: 10.1186/s13045-024-01599-6.
8
METTL3-STAT5B interaction facilitates the co-transcriptional mA modification of mRNA to promote breast tumorigenesis.METTL3-STAT5B 相互作用促进共转录 mA 修饰 mRNA 以促进乳腺癌发生。
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MedComm (2020). 2024 Aug 21;5(9):e702. doi: 10.1002/mco2.702. eCollection 2024 Sep.