BATF (Basic Leucine Zipper ATF-Like Transcription Factor)

Knocking out PD-L1 on EVs reduced Texterm cell infiltration and BATF expression. These findings elucidate an EV-mediated immune evasion axis and reveal actionable targets to overcome immunotherapy resistance.

BATF plays a pivotal role in cervical cancer progression and immune evasion by regulating the STAT1/PD-L1 axis and modulating the tumor immune microenvironment. Targeting BATF, alone or in combination with immune checkpoint inhibitors (PD-L1), represents a promising therapeutic strategy to improve outcomes in cervical cancer patients. Further research is warranted to translate these findings into clinical applications.

Genetic susceptibility to UC significantly correlated with an increased risk of CRC. BATF and JDP2 emerged as key biomarkers in the carcinogenesis of UC. Based on abnormal BATF expression at the single-cell level, Treg cell was identified as important cell involved in UC carcinogenesis.

Moreover, we found that BATF, combined with the jun proto-oncogene, AP-1 transcription factor subunit (JUN), led to the suppression of huntingtin interacting protein 1-related (HIP1R) expression and the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. In conclusion, SLC39A5 promotes the progression of GC via the BATF/HIP1R axis, which suggests that SLC39A5 acts as a therapeutic or diagnostic target for GC.

The comprehensive analysis of BATF family genes that may provide novel insights for prognostic biomarkers and Immunotherapy in CRC.

Transforming growth factor β (TGF-β) signaling and CD103 expression were necessary for Trm-like TIL formation, but BATF overexpression was sufficient to drive formation of CD69+CD103+ TIL in TGFBR2-silenced cells. These findings reveal mechanisms of Trm-like TIL differentiation and provide a framework for considering tissue residency in the context of CD8+ T cell heterogeneity in the tumor microenvironment.

Together, these findings define FL3B and FL/DLBCL as biologically and clinically distinct B-cell lymphomas, differing from traditional FL. FL1-2 and FL3A differ in their tumor microenvironments rather than genetic profiles.

We establish a prognostic model based on BATF, EGR1, PD-1, PD-L1, and TIM-3 expression that effectively predicts survival outcomes for AML patients and allo-HSCT recipients. This model may provide valuable insights for prognosis assessment and treatment strategies.

Finally, there were differences in receptor ligand pairs between AML cells with high and low expression of BATF and immune cells. Bioinformatics analysis and experimental verification revealed that BATF expression could alter the proportions of CD8+T cells and NK cells in AML and affect drug sensitivity, making it a potential treatment target for AML.

The prognostic model comprising ARPC1B, BATF, CCL2, and COTL1 can effectively identify high-risk EC patients and predict their response to immunotherapy, demonstrating significant clinical potential. These genes are implicated in EC development and immune infiltration, with BATF emerging as a potential therapeutic target for EC.

This inhibition leads to suppressed tumor growth and metastasis in prostate cancer models. The findings highlight the promise of nanoparticle-based approaches in modulating Treg cell activity for prostate cancer therapy, offering a potential avenue for precision medicine interventions in combating this prevalent malignancy.

Six characteristic genes (BATF, CXCR3, GIMAP5, GPR18, ISG20, and IGHM) were identified by machine learning, and these genes are associated with multiple immune-related pathways and immune cells in neuroblastoma. BATF, CXCR3, GIMAP5, GPR18, ISG20, and IGHM may serve as biomarkers that reflect the conditions of the immune microenvironment of neuroblastoma and hold promise in guiding neuroblastoma treatment.