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Abstract：
N6-methyladenosine (m6A), the most abundant RNA modification within cells, participates in various biological and pathological processes, including self-renewal, invasion and proliferation, drug resistance, and stem cell characteristics. The m6A methylation plays a crucial role in tumors by regulating multiple RNA processes such as transcription, processing, and translation. Three protein types are primarily involved in m6A methylation: methyltransferases (such as METTL3, METTL14, ZC3H13, and KIAA1429), demethylases (such as FTO, ALKBH5), and RNA-binding proteins (such as the family of YTHDF, YTHDC1, YTHDC2, and IGF2BPs). Various metabolic pathways are reprogrammed in digestive tumors to meet the heightened growth demands and sustain cellular functionality. Recent studies have highlighted the extensive impact of m6A on the regulation of digestive tract tumor metabolism, further modulating tumor initiation and progression. Our review aims to provide a comprehensive understanding of the expression patterns, functional roles, and regulatory mechanisms of m6A in digestive tract tumor metabolism-related molecules and pathways. The characterization of expression profiles of m6A regulatory factors and in-depth studies on m6A methylation in digestive system tumors may provide new directions for clinical prediction and innovative therapeutic interventions.
摘要：
N6-甲基腺苷（m6A），细胞内最丰富的RNA修饰，参与各种生物和病理过程，包括自我更新,入侵和增殖，耐药性,和干细胞特征。m6A甲基化通过调节转录等多种RNA过程在肿瘤中起着至关重要的作用,processing,和翻译。三种蛋白质类型主要参与m6A甲基化：甲基转移酶（如METTL3，METTL14，ZC3H13和KIAA1429），去甲基酶(如FTO，ALKBH5),和RNA结合蛋白（例如YTHDF家族，YTHDC1、YTHDC2和IGF2BPs)。各种代谢途径在消化性肿瘤中被重新编程以满足增加的生长需求并维持细胞功能。最近的研究强调了m6A对消化道肿瘤代谢调节的广泛影响，进一步调节肿瘤的启动和进展。我们的审查旨在全面了解表达模式，功能角色，m6A在消化道肿瘤代谢相关分子和通路中的调控机制。对消化系统肿瘤中m6A调控因子表达谱的表征和m6A甲基化的深入研究可能为临床预测和创新治疗干预提供新的方向。
