The BATF3 Knockout A-549 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of A-549 human lung adenocarcinoma cells with targeted disruption of the BATF3 gene. This heterogeneous knockout pool avoids the clonal selection bias inherent to single-cell-derived lines and captures a range of CRISPR-induced gene modifications, making it suited for robust loss-of-function studies. The product enables systematic exploration of BATF3’s role in cancer cell signaling and immunomodulatory functions without the need for clonal isolation.
The host A-549 cell line was originally established from the lung adenocarcinoma of a 58-year-old White male and exhibits an adherent epithelial morphology with a KRAS mutation. As a well-characterized model for non-small cell lung cancer, A-549 facilitates the study of oncogenic signaling, metastatic behavior, and drug sensitivity. Its genomic stability and compatibility with standard culture conditions make it a reliable platform for gene editing and downstream functional assays.
BATF3 is a basic leucine zipper transcription factor that forms heterodimers with AP-1 components JUN, FOS, and BATF to regulate gene expression. In dendritic cells, BATF3 is essential for lineage commitment and drives IL-12 production, a key mediator of antitumor immunity. Upstream, BATF3 is activated by GM-CSF, FLT3L, IFN-gamma, and Toll-like receptor ligands through pathways involving JAK2, STAT5, IRF8, and PU.1. Downstream targets include co-stimulatory molecules CD80 and CD86, chemokines CXCL9 and CXCL10, and the transcription factor IRF8. In cancer cells, BATF3 modulates AP-1 transcriptional programs that can influence proliferation, survival, and the secretome.
In A-549 lung adenocarcinoma cells, BATF3 knockout disrupts AP-1-driven gene networks, potentially altering the expression of cytokines and immune modulators that contribute to tumor progression and immune evasion. This model allows researchers to dissect the specific contribution of BATF3 to the oncogenic transcriptome and to evaluate how its loss reshapes the cellular response to external stimuli and interactions within the tumor microenvironment.
Applications of these polyclonal knockout cells include transcriptomic profiling by RNA-seq, genome-wide binding analysis by ChIP-seq, and targeted gene expression quantification via RT-qPCR. Functional assays such as proliferation, apoptosis, migration, and invasion can reveal phenotypic consequences of BATF3 disruption, while ELISA-based measurement of cytokines like IL-12 and chemokines such as CXCL9/CXCL10 provides insight into secretory changes. For further technical details and ordering information, please contact Ascent Research.
