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Background.The long non-coding RNA (lncRNA) LINC00969 is involved in human disease progression, and n6-methyladenosine (m 6 A) modification of lncRNAs in cancer has been proven to be a key regulatory mechanism.However, our understanding of its effects and mechanisms of action in papillary thyroid carcinoma (PTC) remains limited.Objectives.This study aimed to elucidate the role of methyltransferase-like 3 (METTL3)-induced m 6 A modification of LINC00969 in PTC tumorigenesis. Materials and methods.Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to analyze LINC00969 and METTL3 mRNA levels in PTC.The regulation of LINC00969 by METTL3 was confirmed using cell function experiments, molecular biology assays and bioinformatics analysis.LINC00969 stabilization analysis was performed to verify the regulatory roles of METTL3 and LINC00969.Results.LINC00969 expression was downregulated in PTC tissues.Increased LINC00969 expression inhibited the invasion, growth and migration of PTC cells.METTL3 downregulation in PTC mediated the m 6 A modification of LINC00969, increasing its stability.Furthermore, METTL3 levels were downregulated in PTC, and its silencing partially reversed the inhibitory effect of LINC00969 overexpression on PTC cell malignancy.Conclusions.LINC00969 overexpression inhibits PTC cell malignancy via METTL3-mediated m 6 A modification.These findings suggest that METTL3-m 6 A-LINC00969 is a promising therapeutic target for PTC.
Huang et al. (Tue,) studied this question.