Knock out of LSM12 Promotes OSCC Ferroptosis via WNT/-catenin Signaling Pathway and NADPH-related Pathways

LSM12 (Like-Sm Protein 12) is a novel tumorigenesis-related gene involved in alternative splicing of USO1 exon 15, but its role in Oral Squamous Cell Carcinoma (OSCC) and ferroptosis regulation is unknown. This study explores the effect of LSM12 on ferroptosis by regulating the WNT/-catenin signaling pathway and the NADPH-related pathways. We assume that LSM12 regulates ferroptosis by affecting these pathways. The prediction results show that LSM12 gene knockout can induce ferroptosis, reduce -catenin expression, and reduce NADK activity, resulting in a decrease in cell vitality. However, some experimental groups did not have the expected change, which may be related to the compensation mechanism or experimental variation. The results of the study support the view that LSM12 regulates ferroptosis through WNT/-catenin and NADPH-related pathways. In short, LSM12 plays an important role in OSCC by regulating ferroptosis, which may provide a new direction for targeted treatment to enhance ferroptosis sensitivity and improve the effectiveness of cancer treatment. Future research needs to further explore the role of LSM12 in other cancer types.