关键词: N6-methyladenosine YTHDF1 cancer cell metabolic reprogramming molecular mechanisms

Mesh : Humans Neoplasms Biomarkers, Tumor Metabolic Reprogramming Protein Biosynthesis Recognition, Psychology RNA-Binding Proteins

来  源:   DOI:10.3390/molecules29010140   PDF(Pubmed)

Abstract:
With the advancement of research on m6A-related mechanisms in recent years, the YTHDF protein family within m6A readers has garnered significant attention. Among them, YTHDF1 serves as a pivotal member, playing a crucial role in protein translation, tumor proliferation, metabolic reprogramming of various tumor cells, and immune evasion. In addition, YTHDF1 also exerts regulatory effects on tumors through multiple signaling pathways, and numerous studies have confirmed its ability to assist in the reprogramming of the tumor cell-related metabolic processes. The focus of research on YTHDF1 has shifted in recent years from its m6A-recognition and -modification function to the molecular mechanisms by which it regulates tumor progression, particularly by exploring the regulatory factors that interact with YTHDF1 upstream and downstream. In this review, we elucidate the latest signaling pathway mechanisms of YTHDF1 in various tumor cells, with a special emphasis on its distinctive characteristics in tumor cell metabolic reprogramming. Furthermore, we summarize the latest pathological and physiological processes involving YTHDF1 in tumor cells, and analyze potential therapeutic approaches that utilize YTHDF1. We believe that YTHDF1 represents a highly promising target for future tumor treatments and a novel tumor biomarker.
摘要:
随着近年来对m6A相关机制研究的进展,m6A阅读器中的YTHDF蛋白家族引起了极大的关注。其中,YTHDF1作为关键成员,在蛋白质翻译中起着至关重要的作用,肿瘤增殖,各种肿瘤细胞的代谢重编程,和免疫逃避。此外,YTHDF1还通过多种信号通路对肿瘤发挥调节作用,和许多研究已经证实了它的能力,以协助重编程的肿瘤细胞相关的代谢过程。近年来,对YTHDF1的研究重点已从其m6A识别和修饰功能转移到其调节肿瘤进展的分子机制。特别是通过探索与YTHDF1上游和下游相互作用的调节因素。在这次审查中,我们阐明了YTHDF1在各种肿瘤细胞中的最新信号通路机制,特别强调其在肿瘤细胞代谢重编程中的独特特征。此外,我们总结了YTHDF1在肿瘤细胞中的最新病理和生理过程,并分析利用YTHDF1的潜在治疗方法。我们相信YTHDF1代表了未来肿瘤治疗的一个非常有希望的靶标和新的肿瘤生物标志物。
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