The BATF3 Knockout SK-OV-3 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian adenocarcinoma epithelial cell line SK-OV-3. This product features targeted disruption of the BATF3 gene, which encodes a basic leucine zipper transcription factor of the AP-1 family, via CRISPR/Cas9-mediated gene disruption. The polyclonal nature provides a heterogeneous pool of cells with diverse knockout alleles, enabling robust loss-of-function studies without clonal variability. This knockout model serves as a versatile tool for investigating BATF3-dependent signaling pathways in an ovarian cancer context.
The SK-OV-3 cell line was originally isolated from the ascites of a patient with ovarian adenocarcinoma and is widely employed as an epithelial tumor model. These cells are p53-deficient and HER2-positive, contributing to their highly tumorigenic phenotype in both in vitro and in vivo settings. The epithelial origin of SK-OV-3 makes it particularly relevant for studying ovarian cancer biology, including metastasis, drug resistance, and interactions with the tumor microenvironment. The BATF3 knockout in this background offers a defined genetic manipulation to explore the intersection of transcription factor networks and ovarian tumorigenesis.
BATF3 is a basic leucine zipper transcription factor that heterodimerizes with c-JUN to regulate gene expression within the AP-1 network. It is transcriptionally regulated by IRF8 and PU.1, and activated by FLT3L, GM-CSF, and IFN-??. BATF3 is essential for CD8??+ dendritic cell development and cross-presentation, directly controlling transcription of IL-12, CXCL10, type I interferons, CD8A, and CCR7. It interacts with IRF4 and IRF8 and functions within a pathway involving STAT1, STAT2, and IRF9, linking AP-1 to type I interferon and TLR signaling. Gene disruption thus impairs a central node in immune activation.
In the SK-OV-3 ovarian cancer background, BATF3 knockout impairs AP-1-mediated transcriptional programs implicated in tumor-immune interactions. Ovarian carcinomas often exploit immune evasion; this model enables dissection of how dendritic cell-related transcription factors shape the immune microenvironment. It can be used to investigate how IL-12 and CXCL10 influence anti-tumor immunity and cross-presentation in ovarian cancer. This model is particularly valuable for examining disrupted interferon responses in a HER2-positive, p53-null epithelial tumor context, revealing potential therapeutic vulnerabilities.
Applications include dendritic cell biology, tumor immunology, AP-1 network analysis, ovarian cancer immune microenvironment modeling, and immunomodulatory drug screening. Assays such as Western blotting, RT-qPCR, MTT proliferation, transwell migration, flow cytometry for apoptosis, and RNA-seq are compatible. This targeted disruption of BATF3 in SK-OV-3 enables advanced studies of transcription factor signaling in immune surveillance. For further information, contact Ascent Research.
