The BATF3 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human NCI-H1703 lung adenocarcinoma epithelial cell line. This product provides targeted disruption of the BATF3 locus, introducing loss-of-function alleles across the cell population. Unlike monoclonal knockout lines, these polyclonal cells retain allelic diversity, making them suitable for experiments that do not require clonal uniformity and for studying heterogeneous knockout phenotypes. The cells are supplied as a ready-to-use reagent for immediate downstream functional assays.
The host NCI-H1703 cell line was established from a lung adenocarcinoma of a male smoker and is characterized by an epithelial morphology and a TP53 mutation. This widely used lung cancer model supports investigations into oncogenic signaling, therapeutic responses, and tumor biology. The TP53-mutant background is particularly relevant for studying genetic dependencies and drug sensitivities in non-small cell lung carcinoma. In the context of BATF3 knockout, this line offers a malignancy-relevant platform to dissect the transcription factor??s roles in cancer cell-autonomous processes and tumor-immune crosstalk.
BATF3 encodes a basic leucine zipper (bZIP) transcription factor that dimerizes with JUN family members (JUN, JUNB, JUND) and cooperates with IRF4 and IRF8 to regulate gene expression. Upstream, BATF3 is induced by FLT3L and GM-CSF signaling through the transcription factors IRF8 and PU.1. Downstream targets include IL12B, CD8A, XCR1, and CLEC9A, which are essential for antigen cross-presentation and T cell activation. In immune cells, BATF3 is indispensable for the development of CD8??+ conventional dendritic cells (cDC1s) and for mounting effective anti-tumor immune responses. The BATF3?CJUN?CIRF8 axis integrates FLT3 receptor signals to promote IL-12 secretion and interferon-gamma (IFNG) production, thereby linking innate and adaptive immunity.
In the NCI-H1703 lung adenocarcinoma model, BATF3 knockout enables investigation of this transcription factor??s roles in a TP53-mutant cancer context. Researchers can examine effects on proliferation, migration, cytokine secretion, and drug sensitivity. Co-culture with immune cells allows assessment of how BATF3 loss in tumor cells influences dendritic cell function, T cell activation, and inflammatory signaling in the tumor microenvironment. The polyclonal nature captures a breadth of functional defects, enhancing robustness of phenotypic screens.
Broad research applications include transcriptomic and proteomic profiling (RNA-seq, mass spectrometry) to define BATF3-regulated networks, RT-qPCR and western blotting for gene expression and protein validation, and cell viability (MTT/XTT) assays for growth phenotypes. Migration and invasion can be measured with transwell systems, and in vivo tumorigenicity assessed via xenograft models in immunocompromised or humanized mice. These tools facilitate drug discovery, tumor immunology studies, and identification of synthetic lethal interactions in TP53-mutant lung adenocarcinoma. For further technical details, please contact Ascent Research.
