Correlations of m6A methylation-related mRNAs with thyroid cancer

N6-methyladenosine (m6A) RNA methylation plays a crucial role in tumorigenesis. However, the specific role of m6A modifications in the malignant progression of papillary thyroid carcinoma (PTC) without autoimmune thyroid disease (AITD) remains unclear. We analyzed a randomly selected subset of three pairs from a total cohort of 26 pairs of cancerous and para-cancerous tissues from patients with PTC without AITD to investigate global m6A levels and the gene expression of key factors driving m6A methylation. Our results revealed a significant increase in global m6A methylation in cancerous tissues, accompanied by upregulation of the m6A "reader" gene IGF2BP2. Of the 486 upregulated and 39 downregulated genes identified in cancerous tissues, most of the top-enriched pathways were associated with activated genes and contributed to cancer progression. A significant protein-protein interaction between IGF2BP2 and several key cancer-related genes, particularly FN1 and LAMB3, was observed. Moreover, 313 mRNAs, 55 lncRNAs, and 8 ncRNAs exhibited significant m6A methylation differences, overlapping with differentially expressed cancer-associated genes, particularly NUM, which was recently identified as a potential biomarker for PTC. These findings underscore the importance of m6A-related mechanisms and functions in PTC without AITD development and suggest that FN1-, NMU-, and LAMB3-associated pathways may be potential therapeutic targets and molecular mechanisms for this disease.