The N6-Methyladenosine-Modified CIT Promotes Uterine Corpus Endometrial Carcinoma Progression by Inhibiting the Hippo Signaling Pathway.

This study investigates the role of CIT gene in uterine corpus endometrial carcinoma (UCEC) progression, focusing on its regulation by m6A methylation. Bioinformatics and experimental analyses (EdU, colony formation assay, Dot blot, MeRIP-PCR, RNA pull-down, qRT-PCR, Western Blotting, apoptosis assay) revealed that CIT was significantly overexpressed in UCEC. Mechanistically, we found that the m6A writer RBM15-mediated CIT mRNA methylation, which was then recognized by the reader IGF2BP1 to enhance CIT mRNA stability and expression. Consequently, this m6A-mediated upregulation of CIT inhibited the Hippo signaling pathway, ultimately suppressing apoptosis and promoting malignant proliferation in UCEC. These findings elucidated a novel RBM15/IGF2BP1-CIT-Hippo axis, providing new theoretical insights and potential therapeutic targets for UCEC.