The BATF3 Knockout A2780 Polyclonal Cells product offers a CRISPR/Cas9-mediated polyclonal knockout population wherein the BATF3 gene is disrupted in the A2780 human ovarian carcinoma cell line. This polyclonal format yields a heterogeneous pool of edited cells with loss-of-function mutations, enabling robust BATF3 deficiency modeling without clonal selection while retaining biological diversity of the parental line.
The A2780 line is a well-established model of human ovarian endometrioid adenocarcinoma, derived from an untreated, platinum-sensitive patient. These adherent epithelial cells maintain key oncogenic features and drug sensitivity profiles, making them ideal for studying tumor cell-autonomous signaling and immune interactions within the ovarian cancer microenvironment.
BATF3 is a transcription factor driving conventional type 1 dendritic cell (cDC1) development. As an AP-1 family member, it partners with JUN and BATF and responds to GM-CSF, FLT3L, and IFN-??, with IRF8 and PU.1 as co-regulators. It transcriptionally activates cDC1 genes IRF8, ID2, ZBTB46, XCR1, and CLEC9A, enabling cross-presentation to CD8+ T cells. This links TLR4/MyD88 and IFNAR/STAT1 pathways to adaptive antitumor immunity.
In A2780 ovarian cancer cells, BATF3 knockout allows study of cDC1-mediated immune surveillance. Although BATF3 acts in dendritic cells, this model can be employed to examine tumor-derived signals influencing cDC1 function or to provide a BATF3-null environment in co-cultures. Loss of BATF3 activity impairs cross-presentation and CD8+ T cell priming, directly relevant for ovarian immunotherapy research.
Key applications encompass investigation of the IRF8/BATF3 regulatory axis, tumor-immune interaction assays, and checkpoint blockade evaluation. This product supports flow cytometry for cDC1 markers, RT-qPCR/western blotting for BATF3 pathway components, cytokine profiling, T cell co-cultures, and transcriptomic analysis. It is suitable for cancer vaccine studies that rely on effective cross-priming. For technical details, contact Ascent Research.
