The BATF3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line, engineered for loss-of-function studies of the BATF3 gene. This polyclonal pool contains heterogeneous gene-disruption profiles, enabling robust assessment of BATF3-dependent phenotypes without clonal selection artifacts. The product provides a flexible platform for investigating BATF3-mediated transcriptional regulation and its impact on cancer cell biology in a widely utilized immortalized cell model.
HeLa cells, isolated from a cervical adenocarcinoma of a 31-year-old African American woman, are HPV18-positive and exhibit a hypertriploid karyotype. This immortalized cell line is a cornerstone of biomedical research, extensively employed in cancer biology, virology, and molecular signaling studies. Their robust proliferation and well-characterized genomic landscape make them an ideal host for CRISPR-based knockout models, facilitating reproducible investigation of gene function in a cervical cancer context.
BATF3 encodes a basic leucine zipper transcription factor that functions by heterodimerizing with Jun family proteins (JUN, JUNB, JUND) and ATF2, and interacts with IRF4 to control gene transcription. It is a master regulator of dendritic cell lineage commitment, driving development of CD8??+ and CD103+ dendritic cells through direct transcriptional activation of ID2 and IRF8. BATF3 activity is regulated by upstream signals including IL-4, GM-CSF, FLT3L, interferon-gamma, and TLR ligands, which converge on receptors such as the GM-CSF receptor, FLT3, and TLRs. Downstream, BATF3 promotes expression of Zbtb46, IL-12, and interferon-gamma-induced genes, thereby integrating cytokine and pathogen-sensing pathways to orchestrate antigen cross-presentation and cytotoxic T cell responses.
Introducing BATF3 disruption in HeLa cells creates a unique experimental system to dissect BATF3??s tumor-intrinsic functions independent of its immunological role in dendritic cells. While HeLa cells do not naturally participate in antigen presentation, they express components of the transcriptional machinery that interacts with BATF3, enabling investigation of how BATF3 influences epithelial cancer cell behavior. This model permits the study of BATF3-mediated gene regulation in a cancerous epithelial background, potentially revealing novel roles in proliferation, survival, or invasion pathways relevant to cervical adenocarcinoma progression.
Researchers can employ this polyclonal knockout model to examine BATF3-dependent transcriptional programs using techniques such as RNA-seq, ChIP-qPCR, and reporter gene assays. Functional consequences of BATF3 loss on cell proliferation, migration, and invasion can be assessed by standard cellular assays, while co-immunoprecipitation and Western blotting enable mapping of BATF3 interaction networks with Jun proteins and other partners. Additionally, the cells serve as a tool for high-throughput screening of small molecules or genetic modifiers that compensate for BATF3 deficiency. For further technical information or to discuss custom applications, please contact Ascent Research.
