UBTF facilitates acute myeloid leukemia development and immune escape via PD-L1 regulation

UBTF has been implicated in the development of multiple cancers, yet its specific biological function in acute myeloid leukemia (AML) remains unclear. This study utilized expression profiles and clinical data from The Cancer Genome Atlas (TCGA) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) databases, with UBTF expression data obtained from the GEPIA database. Analysis via the R software package CIBERSORT explored immune cell infiltration levels under different UBTF expression levels. LASSO Cox analysis with optimized penalty parameters identified genes associated with survival outcomes, leading to the construction of a prognostic risk model using multivariate Cox regression analysis. Prognostic significance was evaluated and validated through Kaplan-Meier survival analysis and receiver operating characteristic curve analysis. Experimental validation using stable AML cell lines with UBTF overexpression or knockdown, transcriptome sequencing, and a CD8 + T cell killing assay were performed. Ultimately, in vivo experimental validation was conducted. Results revealed that UBTF is overexpressed in AML compared to normal tissues and correlates with poor clinical prognosis. UBTF overexpression is associated with increased expression of PD-L1 (CD274) and immune cell infiltration, suggesting its role in promoting AML progression via PD-L1 (CD274)-mediated immune evasion. These findings highlight UBTF as a potential prognostic biomarker and a novel therapeutic target for tumor immunotherapy in AML. • UBTF is highly expressed in AML and associated with poor prognosis. • UBTF promotes immune evasion in AML. • UBTF-mediated immune evasion is linked to CD274 (PD-L1) regulation.