The BATF3 Knockout KYSE-150 Polyclonal Cells product comprises a heterogeneous pool of CRISPR/Cas9-edited KYSE-150 cells carrying targeted disruption of the BATF3 gene. This polyclonal knockout population is generated through genome editing to introduce loss-of-function mutations, creating a versatile model for studying BATF3-dependent processes in an esophageal squamous cell carcinoma background. The product is supplied as a ready-to-use polyclonal cell pool, allowing researchers to bypass clonal isolation and expansion steps while retaining the functional consequences of BATF3 ablation. It is suitable for transient and stable assays in cancer biology, immunology, and drug discovery research.
KYSE-150 is a human esophageal squamous cell carcinoma cell line derived from a poorly differentiated esophageal tumor. These adherent cells exhibit typical epithelial morphology and harbor genomic alterations common in esophageal cancers, including TP53 mutations and chromosomal abnormalities. As a representative model of esophageal squamous cell carcinoma, KYSE-150 retains properties of cancerous esophageal epithelial cells, such as unregulated proliferation, migratory capacity, and altered signaling networks. The use of KYSE-150 as the host cell line provides a clinically relevant context for investigating the role of BATF3 in tumor cell-intrinsic functions and in shaping interactions with the immune microenvironment.
BATF3 encodes a basic leucine zipper (bZIP) transcription factor that heterodimerizes with JUN, IRF4, IRF8, BATF, and MAF family members to regulate gene expression. In dendritic cells, BATF3 is activated by upstream signals including FLT3 ligand, GM-CSF, interferon-gamma, and transcription factors IRF8 and PU.1. Downstream of FLT3 receptor engagement, STAT3 and STAT5 phosphorylation converges on IRF8 and BATF3 induction to drive the commitment of CD8+ dendritic cell lineage. BATF3 directly transcriptionally regulates IL12B and IL23A, genes critical for T-cell polarization and anti-tumor immunity. Through these interactions, BATF3 influences dendritic cell development, interferon signaling, toll-like receptor pathways, and antigen cross-presentation, linking innate and adaptive immune responses.
Loss of BATF3 function in KYSE-150 cells disrupts intrinsic gene expression programs that may contribute to immune evasion in esophageal squamous cell carcinoma. Because BATF3 is normally involved in cytokine production and dendritic cell lineage specification, its deletion in cancer cells may alter the expression of immunomodulatory factors and affect tumor cell behavior. The knockout model enables investigation of how BATF3 deficiency modulates the expression of IL12B, IL23A, and other downstream targets within the tumor cell context. This system is particularly relevant for dissecting how cancer cells co-opt transcriptional networks typically associated with immune cells, potentially uncovering novel mechanisms of immune escape and tumor progression.
This polyclonal BATF3 knockout cell model supports a broad range of applications in dendritic cell biology, immuno-oncology, tumor microenvironment research, and esophageal cancer gene function studies. Researchers can employ western blotting and RT-qPCR to confirm gene disruption, flow cytometry to assess surface marker changes, co-culture assays with immune cells to evaluate cross-talk, and cytokine secretion assays to profile secreted factors. RNA-seq analysis can reveal global transcriptomic alterations, while migration and invasion assays and drug sensitivity testing provide functional readouts. The cells serve as a robust platform for screening compounds that modulate pathways influenced by BATF3 or for validating targets in the JAK-STAT, interferon, and TLR signaling axes. For additional details and ordering information, please contact Ascent Research.
