BATF3 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the MCF-7 human breast adenocarcinoma line, carrying targeted disruption of the BATF3 gene. The polyclonal format consists of a heterogeneous pool of edited cells, offering a robust loss-of-function model while mitigating clonal artifacts. This population enables investigation of BATF3-dependent pathways in a breast epithelial context without the limitations of single-cell clones.
The parental MCF-7 line is an estrogen receptor-positive luminal breast adenocarcinoma model originating from a pleural effusion. These adherent cells retain key features of hormone-responsive disease, including dependence on estrogen for growth, making them a central model for breast cancer biology and endocrine therapy research. Their well-characterized signaling networks and tumorigenic properties provide a reliable background for studying gene function in breast malignancy.
BATF3 is a transcription factor that forms heterodimers with JUN proteins to drive genes essential for dendritic cell development and antigen cross-presentation. It is activated downstream of IFN-?? and IL-12 via STAT4 and IRF8. In the canonical pathway, IL-12 receptor engagement leads to STAT4 phosphorylation, which cooperates with IRF8 to induce BATF3; BATF3 then partners with JUN and IRF8 to regulate targets such as XCR1, IL12B, and CCL5. This IL-12R/STAT4/IRF8/BATF3/JUN axis is critical for CD8??+ dendritic cell function and T cell activation.
Disrupting BATF3 in MCF-7 cells provides a valuable model to explore potential tumor-intrinsic roles of this transcription factor. Although classically associated with immune cells, BATF3 knockout in an epithelial cancer line allows assessment of its influence on cytokine expression, immune modulatory factor secretion, and tumor cell interactions with dendritic cells and T cells. This system helps delineate how breast cancer cells may modulate the tumor microenvironment and immune evasion strategies.
These polyclonal knockout cells empower diverse studies, including tumor immunology, cancer immunotherapy, and the tumor microenvironment. Researchers can employ co-culture with dendritic cells or T cells, combined with ELISA for secreted cytokines and flow cytometry for immune markers, to investigate BATF3-dependent immunomodulation. Quantitative RT-PCR and Western blotting enable verification of target gene changes. The cells also support xenograft models to assess tumor-immune interactions in vivo. For further technical inquiries, please contact Ascent Research.