METTL16 inhibits papillary thyroid cancer tumorigenicity through m < sup > 6 < /sup > A/YTHDC2/SCD1-regulated lipid metabolism

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 A939572 inhibited growth and slowed down lipid metabolism in PTC cells. These results confirm the crucial role of METTL16 in restraining PTC progression through SCD1-activated lipid metabolism in cooperation with YTHDC2. This suggests that the combination of METTL16 and anti-SCD1 blockade might constitute an effective therapy for PTC.PMID:38334797 | PMC:PMC10857971 | DOI:10.1007/s00018-024-05146-x
Source: Cellular and Molecular Life Sciences : CMLS - Category: Cytology Authors: Source Type: research