The BATF3 Knockout HCT 116 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the BATF3 gene. This polyclonal knockout pool is derived from the HCT 116 human colorectal carcinoma cell line and offers a versatile loss-of-function model for investigating BATF3-dependent biological processes. The product is supplied as a heterogeneous population of edited cells, enabling researchers to assess phenotypic consequences of BATF3 ablation in a polyclonal context, which mirrors natural genetic variation and avoids clonal artifacts.
HCT 116 is a well-characterized human male colorectal carcinoma cell line with microsatellite stability (MSS) and a KRAS G13D mutation. These epithelial cells provide a robust colorectal cancer model widely used for drug screening, signaling studies, and tumor biology research. The parental line retains oncogenic pathways relevant to colon cancer and is particularly suited for investigating tumor microenvironment interactions and immune evasion mechanisms.
BATF3 encodes a basic leucine zipper transcription factor that forms heterodimers with JUN family proteins (c-Jun, JunB, JunD) to constitute functional AP-1 complexes. These complexes bind DNA and drive the expression of genes essential for conventional type 1 dendritic cell (cDC1) commitment, notably IRF8, ID2, and ZBTB46. Upstream signaling through receptors such as Flt3 activates STAT3 and STAT5, while Toll-like receptor engagement triggers MyD88-dependent NF-??B cascades, both converging on BATF3 induction. Cooperating with IRF4 and IRF8, BATF3 orchestrates the cDC1 transcriptional network, and its downstream targets like IL-15 and CD8?? are crucial for cross-presentation and CD8+ T cell priming. Disruption of BATF3 therefore abrogates cDC1 development, severely impairing antitumor immune responses.
In the HCT 116 colorectal carcinoma background, BATF3 knockout enables dissection of tumor-immune interplay. Although BATF3 is predominantly studied in hematopoietic cells, its disruption in an epithelial tumor model allows examination of tumor cell-intrinsic BATF3 functions or the effects of BATF3 loss in the microenvironment on dendritic cell-mediated surveillance. This model is valuable for co-culture experiments with immune cells to recapitulate tumor-immune interactions and for functional screens to identify modulators of immunotherapy response.
Typical applications include flow cytometry for dendritic cell surface markers, RT-qPCR for IRF8 and ZBTB46, RNA-seq differential expression analysis, in vitro DC differentiation from bone marrow or monocytes, and co-culture systems for cross-presentation assessment. These cells also support Western blotting for BATF3 and its targets, and tumor growth assays in immunocompetent mice to evaluate immunotherapy efficacy. For further technical information, please contact Ascent Research.
