The role of dual specificity phosphatase 1 in modulating hepatitis B virus-driven liver cancer progression and radiation response

Background: Dual-specificity phosphatase 1 (DUSP1) plays a critical role in cellular stress responses, but its function in hepatitis B virus (HBV)-associated hepatocellular carcinoma (LCC) and radiation therapy remains unclear.This study investigates the effects of DUSP1 on HBV replication, tumor progression, and radiation response in LIC.Materials and Methods: Fifteen HBV-LIC patients and 10 radiation-treated liver tumor patients (20-50 Gy) were included.HepG2.2.15 cells were used to establish DUSP1overexpressing and control groups.DUSP1 expression was assessed via Western blot and quantitative polymerase chain reaction (qPCR).HBV replication markers (HBsAg, HBeAg) were measured by enzyme-linked immunosorbent assay (ELISA).Cell proliferation cell counting Kit-8 (CCK-8), migration/invasion (Transwell), and miR-21 expression were evaluated.Statistical analysis was performed using SPSS 22.0.Results: DUSP1 was significantly downregulated in LIC tissues (P < 0.001) and further suppressed in irradiated patients (P = 0.002).DUSP1 overexpression reduced HBV replication (HBsAg: P = 0.008; HBeAg: P = 0.008) and enhanced radiosensitivity.Overexpression inhibited proliferation, migration, and invasion (P < 0.001) and attenuated radiation-induced miR-21 upregulation (P = 0.004).Conclusion: DUSP1 suppresses HBV replication and tumor progression while enhancing radiation response in LIC, suggesting its potential as a therapeutic target for HBV-associated hepatocellular carcinoma.