BATF Drives Cervical Cancer Progression and Immune Evasion by Regulating the STAT1-PD-L1 Axis.

[BACKGROUND] Cervical cancer progression is driven by immune evasion mechanisms, including PD-L1-mediated suppression of T cell activity. BATF, a transcription factor, has been linked to tumor immunity; cancer remains incompletely understood.

[OBJECTIVE] This study investigates the BATF-STAT1-PD-L1 axis in tumor progression and immune regulation.

[METHODS] BATF expression was analyzed in cervical cancer tissues and cell lines. Functional assays assessed the impact of BATF knockdown on proliferation, apoptosis, autophagy, and migration. STAT1 regulation was examined via chromatin immunoprecipitation and Western blot. PD-L1 expression was measured by flow cytometry. In vivo xenograft models were used to evaluate tumor growth and response to PD-L1 blockade.

[RESULTS] BATF was upregulated in cervical cancer and promoted tumor growth, metastasis, and immune evasion. BATF knockdown suppressed proliferation, enhanced apoptosis and autophagy, and reduced migration. Mechanistically, BATF transcriptionally activated STAT1, which induced PD-L1 expression. BATF suppression enhanced CD8⁺ T cell infiltration and improved the efficacy of PD-L1 blockade in vivo.

[CONCLUSION] BATF promotes cervical cancer progression by modulating STAT1 and PD-L1. Targeting BATF may enhance anti-tumor immunity and improve immunotherapy outcomes.