This product consists of a polyclonal population of 786-O human clear cell renal cell carcinoma cells genetically modified via CRISPR/Cas9 to disrupt the BATF3 gene, creating a loss-of-function model. The polyclonal format preserves editing diversity and avoids clonal artifacts, enabling population-level analyses of BATF3-dependent functions in cancer and immune biology.
The parental 786-O cell line, derived from a human clear cell renal cell carcinoma, harbors a biallelic VHL mutation that leads to constitutive HIF stabilization and a pseudohypoxic phenotype. This VHL-deficient model is widely used to study HIF-driven oncogenesis, metabolic reprogramming, and tumor microenvironment interactions in ccRCC.
BATF3 is a basic leucine zipper transcription factor that heterodimerizes with JUN, JUNB, JUND, or ATF2 to regulate target gene expression. It is essential for the development of cross-presenting dendritic cells, cooperating with IRF4 and IRF8 to drive transcription of IL-12p40, type I interferons, and MHC class I pathway components such as TAP1. Upstream regulators including GM-CSF, FLT3L, IFN-??, and CD40 signaling control BATF3 expression, while downstream targets encompass ID2, IRF4, IRF8, and BATF itself. Through these interactions, BATF3 integrates signals to orchestrate anti-tumor immune responses.
In the VHL-null 786-O renal carcinoma context, BATF3 knockout provides a platform to examine how tumor-intrinsic BATF3 activity intersects with oncogenic HIF signaling to shape the immune phenotype. Although BATF3 is best known in dendritic cells, its expression in epithelial tumors may influence cytokine secretion and antigen presentation machinery. The concurrent HIF stabilization could modulate BATF3 function, potentially affecting IL-12, type I interferon, and MHC-I expression, thereby impacting tumor immune evasion mechanisms. This model thus enables dissection of BATF3-dependent immune-modulatory pathways in a ccRCC-relevant background.
Typical applications include RNA-seq transcriptomic profiling to map BATF3-dependent gene networks, RT-qPCR and Western blotting for BATF3 and targets such as IL-12p40 and IRF4, and ELISA for secreted cytokines. Co-culture assays with T cells or dendritic cells allow assessment of tumor-immune cell communication, while ChIP-qPCR identifies BATF3 genomic binding sites and flow cytometry monitors MHC-I surface expression. These tools make the model suitable for screening immune evasion modulators and investigating crosstalk between HIF and BATF3 signaling. For additional information, please contact Ascent Research.
