Upregulation of CSDE1 mediated by METTL3 facilitates the progression of papillary thyroid cancer via the Wnt/β-catenin pathway

INTRODUCTION: Papillary thyroid carcinoma (PTC) has a high incidence, and identifying key molecules is crucial for improving its treatment.This study aimed to clarify the expression, prognostic value, biological function, and regulatory mechanism of CSDE1 in PTC. MATERIAL AND METHODS: Bioinformatics analysis of TCGA data, RT-qPCR, and western blot assays were used to detect CSDE1/METTL3expression in PTC tissues and cells. CCK-8, colony formation, wound-healing, and Transwell assays were used to evaluate cell phenotypes.MeRIP-qPCR was used to detect m⁶A modification. A dual-luciferase reporter assay was used to confirm regulatory relationships. Pearsoncorrelation analysis was used to evaluate clinical correlations. RESULTS: CSDE1 was highly expressed in PTC and correlated with advanced clinical features and poor prognosis. CSDE1 knockdownsuppressed the proliferation, migration, invasion, and EMT of PTC cells. CSDE1 activated the Wnt/β-catenin pathway. Moreover, METTL3negatively regulated CSDE1 expression via m⁶A modification. CONCLUSIONS: CSDE1 promotes PTC progression through the Wnt/β-catenin pathway under the regulation of METTL3-mediated m⁶A modification, serving as a promising prognostic biomarker and therapeutic target.