m6A修饰与非编码RNA之间的相互调控：在癌症治疗耐药性中的新作用
Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.
作者信息
Fan Dan, Shang Yan, Cong Yating, Jiao Yanlin, Li Na, Zhao Hailong
机构信息
Nanshan Class, The First Clinical Institute, Zunyi Medical University, Zunyi, 563000, China.
Department of Pathophysiology, Zunyi Medical University, Zunyi, 563000, China.
出版信息
Discov Oncol. 2025 May 25;16(1):920. doi: 10.1007/s12672-025-02641-w.
In recent years, the interplay between N6-methyladenosine (mA) modifications and non-coding RNAs (ncRNAs) has emerged as a pivotal research area, owing to their crucial involvement in the pathophysiological mechanisms underlying various diseases. A significant hurdle in cancer therapy is therapeutic resistance, which frequently contributes to adverse patient outcomes. Recent investigations have underscored the vital role that interactions between mA modifications and ncRNAs play in mediating cancer therapeutic resistance via the MAPK, PI3K/Akt/mTOR, Wnt/β-catenin, HIPPO, and NF-κB pathways. This review elucidates how these interactions drive tumor therapeutic resistance by modulating these pathways. By dissecting the regulatory dynamics between mA and ncRNAs in the context of cancer therapeutic resistance, this review aims to deepen the understanding of m6A-ncRNA interaction in cancer therapeutic resistance and identify potential therapeutic targets to improve cancer treatment efficacy.
近年来，N6-甲基腺苷（m⁶A）修饰与非编码RNA（ncRNA）之间的相互作用已成为一个关键的研究领域，因为它们在各种疾病的病理生理机制中起着至关重要的作用。癌症治疗中的一个重大障碍是治疗耐药性，这常常导致患者预后不良。最近的研究强调了m⁶A修饰与ncRNA之间的相互作用在通过丝裂原活化蛋白激酶（MAPK）、磷脂酰肌醇-3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白（PI3K/Akt/mTOR）、Wnt/β-连环蛋白、HIPPO和核因子κB（NF-κB）信号通路介导癌症治疗耐药性中所起的重要作用。本综述阐明了这些相互作用如何通过调节这些信号通路来驱动肿瘤治疗耐药性。通过剖析癌症治疗耐药性背景下m⁶A与ncRNA之间的调控动态，本综述旨在加深对m⁶A-ncRNA相互作用在癌症治疗耐药性中的理解，并确定潜在的治疗靶点以提高癌症治疗效果。
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