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.
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.
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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