COL1A1, mediated by m6A methylation of METTL3, facilitates oral squamous cell carcinoma cell growth and metastasis.

Collagen type I alpha1 (COL1A1) has been found to be abnormal expressed in oral squamous cell carcinoma (OSCC) tissues, but its role and mechanism in OSCC need to be further elucidated. The expression levels of COL1A1 and methyltransferase-like 3 (METTL3) were measured by quantitative real-time PCR and western blot. Cell growth and metastasis were determined by CCK8, colony formation, EdU, flow cytometry and transwell assays. MeRIP, Co-IP and dual-luciferase reporter assays were performed to explore the interplay of COL1A1 and METTL3. COL1A1 mRNA stability was confirmed by Actinomycin D assay. Mice xenograft models were constructed to perform in vivo experiments. COL1A1 and METTL3 were upregulated in OSCC. COL1A1 knockdown suppressed OSCC cell growth and metastasis, while its overexpression had an opposite effect. The stability of COL1A1 mRNA was regulated by the m6A methylation of METTL3. METTL3 overexpression promoted OSCC cell growth and metastasis, and its knockdown-mediated OSCC cell function inhibition could be abolished by COL1A1 overexpression. Besides, silencing of METTL3 reduced OSCC tumor growth by reducing COL1A1 expression. METTL3-stabilized COL1A1 promoted OSCC progression, providing an exact molecular target for the treatment of OSCC.