YTHDF1

YTHDF1 (YTH N6-methyladenosine RNA Binding Protein 1) is a major m⁶A reader that recognizes N⁶-methyladenosine-modified transcripts and promotes the translation of methylated mRNAs, thereby regulating post-transcriptional gene expression and protein synthesis.^[1][4] Mechanistically, YTHDF1 enhances the translational efficiency of its target transcripts through interactions with the translation machinery and translation initiation factors, making it a central effector of m⁶A-dependent gene regulation.^[1][5][6] Beyond its role in RNA metabolism, YTHDF1 participates in immune regulation, where m⁶A-dependent YTHDF1 activity controls antigen-related responses and contributes to antitumor immunity pathways.^[5] In disease contexts, elevated YTHDF1 expression has been reported across multiple malignancies, including ovarian, gastric, colorectal, hepatocellular, and lung cancers, where it promotes tumor growth, metastasis, stemness, or therapeutic resistance through enhanced translation of oncogenic targets.^{[1][2][3][9][10]} Representative downstream effectors include EIF3C, USP14, FZD7, and YAP, which link YTHDF1-mediated translational control to cancer progression and cellular adaptation.^[1][2][3][9] Compared with related YTH-domain family members, YTHDF1 is primarily characterized by its translation-promoting activity, whereas YTHDF2 is widely associated with mRNA decay and degradation pathways, highlighting a functional distinction frequently exploited in mechanistic studies of m⁶A signaling.^[5][11] Consequently, genetic silencing or functional inhibition of YTHDF1 is widely used in experimental models to investigate m⁶A-dependent translation, tumor biology, immune regulation, and therapeutic target validation.^[5][10]