METTL16 inhibits papillary thyroid cancer tumorigenicity through m⁶A/YTHDC2/SCD1-regulated lipid metabolism.

ABSTRACT: Papillary thyroid carcinoma (PTC) stands as the leading cancer type among endocrine malignancies, and there exists a strong correlation between thyroid cancer and obesity. However, the clinical significance and molecular mechanism of lipid metabolism in the development of PTC remain unclear. In this study, it was demonstrated that the downregulation of METTL16 enhanced lipid metabolism and promoted the malignant progression of PTC. METTL16 was expressed at lower levels in PTC tissues because of DNMT1-mediated hypermethylation of its promoter. Loss- and gain-of-function studies clarified the effects of METTL16 on PTC progression. METTL16 overexpression increased the abundance of m⁶A in SCD1 cells, increasing RNA decay via the m⁶A reader YTHDC2. The SCD1 inhibitor A9395

SUBMITTER: Li Q 

PROVIDER: S-EPMC10857971 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature