목적: Sirtuin 6 (Sirt6) is a member of the NAD+-dependent deacetylase family, known to regulate aging, metabolism, and tumorigenesis. While its tumor- suppressive role has been explored in various cancers, its specific function in Schwannoma remains unclear. This study investigates the role of Sirt6 in Schwannoma, focusing on its regulation of reactive oxygen species (ROS) and interaction with Sirtuin 1 (Sirt1). 방법:Schwannoma cells (HEI-193) were subjected to Sirt6 overexpression and knockdown experiments. Key assays, including Western blot, flow cytometry, ROS measurement, apoptosis assay, and in vivo xenograft mouse models, were utilized to analyze the effects of Sirt6 modulation. The relationship between Sirt6, Sirt1 suppression, and ROS generation was further explored. 결과:Sirt6 overexpression significantly increased ROS levels and apoptosis in Schwannoma cells while reducing cell proliferation. Sirt6-induced suppression of Sirt1 was identified as a critical mechanism for ROS- mediated apoptosis. Conversely, Sirt6 knockdown resulted in enhanced tumor growth and reduced ROS levels. In vivo studies corroborated these findings, showing that Sirt6 overexpression suppressed Schwannoma tumor growth and induced apoptosis via increased oxidative stress. 결론:This study demonstrates that Sirt6 acts as a tumor suppressor in Schwannoma by modulating ROS levels and suppressing Sirt1. These findings provide new insights into the molecular mechanisms of Schwannoma pathogenesis and highlight Sirt6 as a potential therapeutic target for Schwannoma management.