Abstract
OBJECTIVES: FBXO22, a member of the F-box family, plays a crucial role in cancer development and progression. However, its expression and biological functions in esophageal cancer (ESCA) remain poorly understood. METHODS: In this study, we investigated FBXO22 expression in ESCA cancer tissues using immunohistochemistry and Western blot analyses. Functional assays, including CCK-8, flow cytometry, Western blot, scratch healing, and Transwell migration and invasion assays, were employed to evaluate the effects of FBXO22 modulation on ESCA cell viability, apoptosis, migration, and invasion. Additionally, a nude mouse model was used to assess the impact of FBXO22 silencing on tumor growth. RESULTS: We found that FBXO22 expression was upregulated in ESCA tissues compared to normal tissues. Silencing FBXO22 inhibited ESCA cell viability, migration and invasion while promoting apoptosis. Conversely, FBXO22 overexpression had the opposite effects. Mechanistically, FBXO22 was found to influence the WNT/β-catenin signaling pathway, and its silencing retarded tumor growth in vivo. CONCLUSIONS: Our findings highlight the critical role of FBXO22 in ESCA progression and suggest it as a potential therapeutic target for ESCA.