The BATF3 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS human gastric adenocarcinoma epithelial cells, engineered to disrupt the BATF3 gene. This pooled polyclonal format provides a stable loss-of-function model without clonal expansion artifacts, enabling reliable investigation of BATF3-dependent processes in a reproducible epithelial context.
The AGS cell line, originally established from a 54-year-old female gastric adenocarcinoma patient, is a widely used epithelial model for gastric cancer. These adherent cells retain hallmark oncogenic pathways and epithelial morphology, offering a clinically relevant platform for studying tumor cell signaling, cytokine responses, and interactions with the immune microenvironment. This background is well-suited for dissecting gene function in gastric adenocarcinoma pathogenesis.
BATF3 encodes a basic leucine zipper transcription factor essential for CD8??+ and CD103+ dendritic cell development. It functions downstream of GM-CSF and Flt3L cytokine stimulation, which activate JAK2/TYK2 and STAT3/STAT5 signaling to induce BATF3 expression. BATF3 partners with IRF8 and PU.1, and forms heterodimers with JUN, JUNB, and JUND to regulate a network of targets including ID2, IRF8, BCL6, IL-12, CXCL10, and type I interferons. It also integrates IFN-?? signals via upstream regulators STAT3 and STAT5. Through these interactions, BATF3 coordinates dendritic cell lineage commitment, cross-presentation, and anti-tumor immune responses.
In AGS gastric adenocarcinoma cells, BATF3 knockout reveals its role beyond immune lineages. AGS cells express GM-CSF and IFN-?? receptors, enabling direct assessment of BATF3-mediated transcriptional responses in an epithelial tumor context. This model is valuable for exploring how gastric cancer cells utilize immune-regulatory transcription factors to modulate inflammatory signaling, interferon responses, and potential immune evasion mechanisms, thus bridging oncogenic and innate immune pathways.
This knockout model supports diverse assays including western blotting, RT-qPCR, RNA-seq, and flow cytometry for phenotypic characterization. Co-immunoprecipitation and ChIP-qPCR can probe BATF3 protein complexes and DNA binding at regulatory regions. Functional studies such as cytokine secretion profiling and T-cell activation assays enable evaluation of immunomodulatory effects. Applications span dendritic cell biology, anti-tumor immunity, gastric cancer immunology, and immune checkpoint research. For additional technical details, please contact Ascent Research.
