suppression of glioblastoma proliferation by inducing oxidative stress via modulation of txndc12 expression

Background: glioblastoma (gbm) is characterized by an unfavorable prognosis and a mere 5.8% 5-year survival rate. the balance between oxidation and reduction within gbm plays a crucial role in its onset and progression, yet the underlying mechanisms remain unclear. objectives: this study aimed to investigate the role of the sulfoxide-domain containing protein 12 (txndc12) in maintaining the oxidation-reduction equilibrium within gbm cells. methods: bioinformatics analysis was employed to assess the significance of txndc12. knockdown experiments on u251 and a172 cells to evaluate the impact on cell proliferation in vitro. additionally, in vivo experiments with stable a172 cells to measure tumor growth reduction. results: the findings indicate that perturbing txndc12 expression through knockdown impeded the proliferation of u251 and a172 cells in vitro. mechanistic investigations revealed that reducing txndc12 expression led to an imbalance in the oxidation-reduction dynamics of gbm. conclusions: this study highlights txndc12 as a potential therapeutic target for gbm. inducing an imbalance in tumor cell oxidation-reduction processes may represent a novel strategy for advancing cancer treatment.