목적: One of the major side effects of cisplatin chemotherapy is hearing loss. Although apoptosis causes cell death primarily in cisplatin-induced ototoxicity, the exact mechanism behind the ototoxic effects of cisplatin is not fully understood. Autophagy is generally known a pro-survival mechanism that protects cells under starvation or stress conditions. However, recent research has reported that autophagy also plays a functional role in cell death. This study aimed to investigate the role of autophagy in cisplatin-induced ototoxicity in an auditory cell line. 방법:Cultured HEI-OC1 cells were exposed to 30 μM cisplatin for 48 h, and cell viability was determined using MTT assays. To evaluate whether autophagy serves to cell death after cisplatin exposure, western blotting and immunofluorescence staining for LC-II were performed. Markers of two autophagy-related pathways were also investigated mTOR and class III PI3K. 결과:The formation of the autophagic protein LC3-II in response to 30 μM cisplatin increased with time. The early upregulation of autophagy exerted cytoprotective activity via the class III PI3K pathway. The late increase in autophagy induced cell death by suppressing the mTOR pathway. 결론:Our results provide evidence that autophagy could induce cell death during cisplatin-induced ototoxicity and that modulating the autophagic pathway might be another strategy against cisplatin- induced ototoxicity.