Hnrnpc Promotes Oscc Progression Through Sod2 Regulation

Oral Squamous Cell Carcinoma (OSCC) has a poor prognosis with a 5-year survival rate of only about 50%. Abnormal energy metabolism is a hallmark of cancer, and m6A RNA methylation is closely related to tumorigenesis. We utilized RNA sequencing and RIP-seq to identify the interaction between HNRNPC and SOD2 mRNA. The effects of HNRNPC and SOD2 on OSCC cell migration, invasion, and energy metabolism were assessed using Western blot, Transwell assays, and Seahorse metabolic analysis. The clinical significance of HNRNPC and SOD2 expression was evaluated in 168 OSCC patient samples through immunohistochemistry and Kaplan-Meier survival analysis. Additionally, a murine model of in situ oral squamous cell carcinoma was employed to validate the therapeutic potential of HNRNPC knockdown combined with anti-PD-L1 treatment. HNRNPC was found to promote OSCC cell migration, invasion, and EMT by upregulating SOD2 expression in an m6A-dependent manner. This interaction enhanced mitochondrial respiration and glycolysis, providing energy for OSCC progression. High expression of HNRNPC and SOD2 in clinical samples correlated with poor prognosis. In vivo experiments demonstrated that HNRNPC knockdown inhibited tumor growth and enhanced the efficacy of anti-PD-L1 therapy. Our findings highlight the critical role of HNRNPC in OSCC progression through the regulation of SOD2 expression and energy metabolism. The HNRNPC-SOD2 axis may serve as a potential therapeutic target for OSCC, warranting further investigation for clinical applications.