Nsun7 Regulates Oscc Ferroptosis Via M5c Methylation

To investigated the biological function of m5C modification in OSCC, explored its potential regulatory mechanisms, providing new therapy for OSCC. OSCC cell lines sensitive to ferroptosis were screened through in vitro experiments to identify relevant m5C regulatory molecule, and the differences in NSUN7 and YBX1 expression between OSCC and normal tissues were assessed. The effects of NSUN7, NF2, and YBX1 on OSCC ferroptosis and progression were studied through both in vitro and in vivo experiments. RNA-bisulfite seq, RNA-seq RNA immunocoprecipitation(RIP) assays, dual-luciferase reporter assays, and actinomycin D assays were utilized to explore the downstream mechanisms of m5C-ferroptosis regulation. The expression of NSUN7 was higher in OSCC tissues compared to normal tissues. Functional experiments demonstrated that knockdown of NSUN7, NF2, or YBX1 in OSCC could induce a decrease in GPX4, thereby inhibiting OSCC progression via ferroptosis pathways. Mechanistic studies indicated that NSUN7 enhances the stability of NF2 mRNA by increasing its m5C modification, thereby promoting the progression of OSCC. Our study unveils a novel regulatory network involving NSUN7, YBX1, and NF2, which modulates ferroptosis in OSCC through RNA methylation. This discovery not only improved our understanding of ferroptosis manipulation network in cancer but also highlights the potential of targeting RNA modifications as a therapeutic strategy.