BATF3 Knockout T-47D Polyclonal Cells comprise a polyclonal population of T-47D human breast cancer epithelial cells engineered via CRISPR/Cas9-mediated disruption of the BATF3 gene. This product provides a loss-of-function model system for investigating the biological roles of the BATF3-encoded basic leucine zipper transcription factor in an estrogen receptor-positive (ER+) and progesterone receptor-positive (PR+) mammary carcinoma background. The polyclonal format preserves heterogeneous gene-editing events across the cell population, enabling robust assessment of BATF3-dependent phenotypes without single-cell cloning artifacts.
The host cell line, T-47D, was originally isolated from a pleural effusion metastasis of a human mammary ductal carcinoma. These cells are ER+ and PR+, while lacking HER2 amplification, making them a widely used model for luminal A subtype breast cancer. T-47D cells exhibit hormone-dependent growth and commonly harbor mutations in the PIK3CA gene, providing context for studying endocrine therapy resistance and tumor progression mechanisms.
BATF3 (Basic Leucine Zipper ATF-Like Transcription Factor 3) encodes a transcription factor that forms obligate heterodimers with JUN family proteins (JUN, JUNB, JUND) to bind AP-1 or AICE motifs and regulate gene expression. This factor is essential for development of conventional type 1 dendritic cells and for cross-presentation of antigens. BATF3 is activated downstream of cytokines such as FLT3L, GM-CSF, and interferon-gamma, and it transcriptionally regulates targets including ID2, IRF8, and key immune mediators like IL-12 and CXCL10. Its interaction with IRF4 and IRF8 defines immune cell differentiation programs. Within JAK-STAT and MAPK signaling, BATF3/JUN heterodimers integrate signals to control cell cycle progression and apoptosis.
In the T-47D breast cancer context, BATF3 knockout may disrupt immune-related gene expression programs and alter cell proliferation, survival, and responses to cytokine stimulation. Given the emerging roles of BATF3 in tumor immunology and its potential involvement in modulating the tumor microenvironment, this polyclonal knockout model facilitates dissection of BATF3-dependent mechanisms in hormone-responsive breast cancer cells. Loss of BATF3 could affect downstream effectors such as IL-12 and CXCL10, impacting both cell-intrinsic tumorigenic properties and paracrine signaling.
Researchers can employ these polyclonal BATF3 knockout cells in diverse experimental workflows including RT-qPCR and western blotting to confirm target disruption, RNA-seq and ChIP-seq for transcriptomic and genomic analyses, flow cytometry for apoptosis and immune marker profiling, and functional assays such as migration, invasion, and colony formation. Cytokine ELISA and co-immunoprecipitation enable exploration of BATF3 interactomes and downstream signaling. This model supports investigations into breast cancer biology, dendritic cell-based immunotherapies, and immune modulation. For further information, contact Ascent Research.
