Abstract
In this study, we investigated the impact of FOXN3 on esophageal cancer progression and its underlying mechanism. Through online databases, we observed a significant decrease in FOXN3 levels in esophageal cancer tissues and EC9706 cells. Conversely, SIRT1 expression was elevated in EC109 and EC9706 cells. FOXN3 was found to interact with SIRT1, AKT1, and PIK3CA. To explore FOXN3′s effects, we treated EC9706 cells with pcDNA-FOXN3, which led to increased FOXN3 levels. Consequently, SIRT1, p-AKT/AKT, p-PI3K/PI3K ratios, cell proliferation,migration, invasion, and expression of Ki67, PCNA, MMP3, MMP9, N-cadherin, Vimentin, and Bcl-2 were reduced. In contrast, cell apoptosis, E-cadherin, and Bax levels increased. Further analysis revealed that FOXN3 inhibited cell proliferation and epithelial-mesenchymal transition (EMT) while promoting apoptosis by down-regulating the SIRT1/PI3K/AKT pathway. In conclusion, FOXN3 plays a crucial role in esophageal cancer progression by modulating the SIRT1/PI3K/AKT pathway, affecting cell proliferation, EMT, and apoptosis. This study highlights FOXN3 as a potential target for therapeutic interventions in esophageal cancer.
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