<b>AKR1C1 promotes esophageal squamous cell carcinoma progression and is associated with </b><b>β</b><b>-catenin signaling and immune-related alterations</b>

In ESCC, AKR1C1 was markedly overexpressed and correlated with unfavorable survival. Pan‑cancer immune profiling revealed that AKR1C1 correlated with reduced CD8+ T cell infiltration alongside enrichment of M2 macrophages and cancer-associated fibroblasts. Focusing on ESCC, high AKR1C1 expression was linked to an immunosuppressive microenvironment, characterized by decreased immune effector cells and downregulation of MHC class I and co‑stimulatory pathways.

In vitro, AKR1C1 knockdown suppressed ESCC cell proliferation, migration, invasion and colony formation, whereas its overexpression produced opposite effects. Mechanistically, AKR1C1 modulated epithelial-mesenchymal transition markers, cyclin D1 and β‑catenin nuclear translocation. Immunohistochemistry validated AKR1C1 overexpression and its prognostic significance in ESCC.</p><p dir="ltr"><b>Conclusion:</b> AKR1C1 is associated with prognosis, tumor progression and an immunosuppressive phenotype in ESCC, supporting its therapeutic potential.</p>