Abstract / Summary
Abstract Objective : Epithelial ovarian cancer (EOC) is characterized by extensive invasive and metastatic potential, yet the molecular mechanisms underlying these aggressive features remain incompletely understood. This study aimed to define the role of quiescin sulfhydryl oxidase 1 (QSOX1) in EOC progression and to determine whether claudin-1 (CLDN1) contributes to QSOX1-mediated epithelial-mesenchymal transition (EMT) and invasive phenotypes. Results : QSOX1 expression was elevated in both EOC tissues and serum compared with nonmalignant controls. Within the tissue cohort, higher QSOX1 expression was observed in patients with advanced-stage disease and was associated with shorter OS. Functionally, QSOX1 promoted tumor cell proliferation, clonogenic growth, migration, and invasion, suppressed apoptosis, and enhanced xenograft tumor growth. Transcriptomic profiling and molecular validation demonstrated that changes in QSOX1 expression were accompanied by corresponding alterations in CLDN1 and EMT-related markers. Moreover, modulation of CLDN1 expression partially reversed the migratory and invasive phenotypes induced by altered QSOX1 expression. Conclusion : These findings suggest that QSOX1 promotes the migration and invasion of EOC cells, accompanied by EMT-related phenotypic changes, and this process is associated with CLDN1.The results provide an experimental basis for further investigation of QSOX1 as a potential therapeutic target in EOC.