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m6A甲基化在肺癌靶向治疗耐药中的作用。

The role of m6A methylation in targeted therapy resistance in lung cancer.

作者信息

Xue Huange, Ma Yufei, Guan Kaiwen, Zhou Yueyang, Liu Yang, Cao Fei, Kang Xiaohong

机构信息

Department of Radiation Oncology, The First Affiliated Hospital of Xinxiang Medical University Xinxiang, Henan, China.

Life Science Research Center, The First Affiliated Hospital of Xinxiang Medical College Xinxiang, Henan, China.

出版信息

Am J Cancer Res. 2024 Jun 15;14(6):2994-3009. doi: 10.62347/LXOS2662. eCollection 2024.

DOI:10.62347/LXOS2662
PMID:39005690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11236795/
Abstract

Targeted therapies have greatly improved clinical outcomes for patients with lung cancer (LC), but acquired drug resistance and disease relapse inevitably occur. Increasingly, the role of epigenetic mechanisms in driving acquired drug resistance is appreciated. In particular, N6-methyladenosine (m6A), one of the most prevalent RNA modifications, has several roles regulating RNA stability, splicing, transcription, translation, and destruction. Numerous studies have demonstrated that m6A RNA methylation can modulate the growth and invasion of cancer cells as well as contribute to targeted therapy resistance in LC. In this study, we outline what is known regarding the function of m6A in the acquisition of targeted therapy resistance in LC.

摘要

靶向治疗极大地改善了肺癌（LC）患者的临床结局，但不可避免地会出现获得性耐药和疾病复发。表观遗传机制在驱动获得性耐药中的作用越来越受到重视。特别是，N6-甲基腺苷（m6A）作为最普遍的RNA修饰之一，在调节RNA稳定性、剪接、转录、翻译和降解方面具有多种作用。大量研究表明，m6A RNA甲基化可调节癌细胞的生长和侵袭，并导致LC中的靶向治疗耐药。在本研究中，我们概述了关于m6A在LC获得靶向治疗耐药中的功能的已知情况。

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本文引用的文献

1
FTO facilitates cancer metastasis by modifying the mA level of FAP to induce integrin/FAK signaling in non-small cell lung cancer.FTO 通过修饰 FAP 的 mA 水平来促进癌症转移，从而诱导非小细胞肺癌中的整合素/FAK 信号通路。
Cell Commun Signal. 2023 Nov 2;21(1):311. doi: 10.1186/s12964-023-01343-6.
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Enhancement of TKI sensitivity in lung adenocarcinoma through m6A-dependent translational repression of Wnt signaling by circ-FBXW7.通过 circ-FBXW7 介导的 m6A 依赖的翻译抑制作用增强肺腺癌对 TKI 的敏感性。
Mol Cancer. 2023 Jul 1;22(1):103. doi: 10.1186/s12943-023-01811-0.
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Molecular alterations of driver genes in non-small cell lung cancer: from diagnostics to targeted therapy.非小细胞肺癌驱动基因的分子改变：从诊断到靶向治疗
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Serum exosomal m6A demethylase FTO promotes gefitinib resistance in non-small cell lung cancer by up-regulating FLRT3, PTGIS and SIRPα expression.血清外泌体 m6A 去甲基化酶 FTO 通过上调 FLRT3、PTGIS 和 SIRPα 的表达促进非小细胞肺癌对吉非替尼的耐药性。
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HNRNPA2B1-mediated mA modification of lncRNA MEG3 facilitates tumorigenesis and metastasis of non-small cell lung cancer by regulating miR-21-5p/PTEN axis.HNRNPA2B1 介导的长非编码 RNA MEG3 的 mA 修饰通过调节 miR-21-5p/PTEN 轴促进非小细胞肺癌的发生和转移。
J Transl Med. 2023 Jun 12;21(1):382. doi: 10.1186/s12967-023-04190-8.
6
The role of regulators of RNA mA methylation in lung cancer.RNA mA甲基化调节因子在肺癌中的作用。
Genes Dis. 2022 Jan 29;10(2):495-504. doi: 10.1016/j.gendis.2021.12.017. eCollection 2023 Mar.
7
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Nat Rev Clin Oncol. 2023 Aug;20(8):507-526. doi: 10.1038/s41571-023-00774-x. Epub 2023 May 23.
8
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Adv Sci (Weinh). 2023 Jul;10(20):e2206744. doi: 10.1002/advs.202206744. Epub 2023 May 12.
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