Activation of Wnt/β-catenin signaling to increase BMI1 by Licl attenuates the toxicity of cisplatin in the HEI-OC1 auditory cells

Cisplatin is a very effective anti-tumor drug; nonetheless, it can induce cochlear hair cell apoptosis and ototoxicity in large doses. WNT/β-catenin signaling is also closely related to aging, embryonic development, and apoptosis. We establish a cisplatin-induced HEI-OC1 auditory cells model. WNT/β-catenin was activated by GSK3 inhibitor Licl to detect the expression level of each component of the WNT pathway and BMI1. The expression of BMI1 in the hair cell line model of HEI-OC1 cells induced by cisplatin was significantly reduced, and cell apoptosis was significantly reduced by increasing the expression level of cell line BMI through activating WNT/β-catenin signaling. Activation of WNT/β-catenin signaling to increase BMI1 expression can reduce the apoptosis of cochlear hair cells induced by cisplatin. BMI1 also has a protective effect on the ototoxicity of cisplatin.