靶向治疗极大地改善了肺癌（LC）患者的临床结果，但不可避免地会发生获得性耐药和疾病复发。人们越来越认识到表观遗传机制在驱动获得性耐药性中的作用。特别是，N6-甲基腺苷 (m6A) 是最常见的 RNA 修饰之一，具有调节 RNA 稳定性、剪接、转录、翻译和破坏的多种作用。大量研究表明，m6A RNA 甲基化可以调节癌细胞的生长和侵袭，并导致 LC 的靶向治疗耐药。在本研究中，我们概述了有关 m6A 在获得 LC 靶向治疗耐药性中的功能的已知信息。AJCR 版权所有 © 2024。

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.AJCR Copyright © 2024.