The BATF3 Knockout TE1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from the human esophageal squamous carcinoma TE1 cell line, with targeted disruption of the BATF3 gene. This heterogeneous pool contains a spectrum of edited alleles, generating a loss-of-function model suitable for dissecting BATF3-dependent processes without the selective pressure or clonal artifacts inherent to single-cell-derived lines. The polyclonal format preserves genetic diversity while ensuring robust gene ablation across the population, providing a reliable platform for functional studies.
The TE1 cell line originates from a poorly differentiated human esophageal squamous cell carcinoma (ESCC), one of the most prevalent and aggressive gastrointestinal cancers. TE1 cells retain key oncogenic features, including activation of MAPK, JAK-STAT, and NF-??B pathways, and express a repertoire of immune-modulatory molecules. As a well-characterized ESCC model, TE1 is widely employed to investigate tumor proliferation, invasion, apoptosis, and interactions with the tumor microenvironment.
BATF3 encodes a basic leucine zipper transcription factor that forms obligate heterodimers with AP-1 family members (JUN, JUNB, JUND) and cooperates with IRF4 and IRF8 to orchestrate gene expression. Its transcriptional activity is induced by cytokines such as IL-4, GM-CSF, and IFN??, as well as by Toll-like receptor (TLR) ligands (LPS, CpG), acting through upstream adaptors MyD88 and kinases that activate NF-??B, STAT1, and STAT3. BATF3 directly targets promoters and enhancers of immune effector genes, including IL12B, IL23A, PD-L1 (CD274), IDO1, and the chemokines CCL5 and CXCL10, thereby shaping the immune landscape. In the TE1 context, BATF3 likely promotes an immunosuppressive transcriptional program that facilitates tumor immune evasion.
Disruption of BATF3 in TE1 cells is predicted to downregulate key immune checkpoint molecules and chemokines, potentially restoring antitumor immunity and attenuating malignant properties. This knockout model enables dissection of the tumor-intrinsic role of BATF3 in regulating PD-L1 and IDO1 expression, as well as cytokine and chemokine secretion profiles. By removing BATF3-mediated transcriptional control, researchers can interrogate how loss of this factor alters signaling through AP-1 and STAT-dependent cascades and modifies the crosstalk with immune cells in the ESCC microenvironment.
This polyclonal product is designed for a broad spectrum of experimental applications, including transcriptomic profiling by RNA-seq or RT-qPCR, immunoblotting to confirm BATF3 depletion and target modulation, flow cytometry and cytokine ELISA to quantify immune mediators such as PD-L1 and CCL5, and co-culture assays with T cells to evaluate tumor immune evasion. Additional functional assays??transwell migration, MTT viability, and luciferase reporter systems??can be employed to assess effects on invasion, proliferation, and transcriptional activity. The polyclonal knockout cells serve as an ideal tool for AP-1 pathway analysis, drug screening, and mechanistic studies of ESCC immune escape. For further information, please contact Ascent Research.
