BATF3 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1, designed to disrupt the BATF3 gene. This heterogeneous pool offers a loss-of-function model reflecting natural genetic variability, suitable for robust functional studies without clonal artifacts. The CRISPR/Cas9-mediated gene disruption targets the BATF3 locus, enabling investigation of its role in malignant epithelial cells.
SK-HEP-1 is a widely used human liver adenocarcinoma cell line with malignant epithelial characteristics, established from the ascites of a patient with hepatic adenocarcinoma. It serves as a well-characterized model for hepatocellular carcinoma research, exhibiting adherent growth and aneuploid karyotype. The cell line retains active signaling pathways central to hepatocarcinogenesis and tumor biology, providing a relevant backdrop for dissecting BATF3 functions.
BATF3 encodes a basic leucine zipper transcription factor essential for cross-presenting dendritic cell development. It cooperates with IRF8 to regulate downstream targets such as ID2 and ZBTB46, forming the BATF3-IRF8-ID2 axis. This pathway is stimulated by upstream cytokines including FLT3L, GM-CSF, and type I interferons via FLT3-FLT3-STAT3/5 and IFN-??/?? signaling. BATF3 interacts with JUNB, ATF4, BATF, and NFIL3, integrating immune signals to promote CD8+ T cell priming and anti-tumor immunity.
In the SK-HEP-1 liver cancer background, BATF3 knockout allows exploration of this transcription factor??s potential non-canonical roles beyond dendritic cells. While BATF3 is predominantly studied in immunity, its disruption in hepatic adenocarcinoma cells can reveal contributions to cell-autonomous behaviors such as interferon responsiveness, tumor cell immunogenicity, and manipulation of the immune microenvironment. This model thus bridges immuno-oncology and liver cancer fields, enabling the study of tumor-intrinsic immune modulation.
These polyclonal knockout cells are suited for western blotting and RT-qPCR to confirm BATF3 loss and monitor downstream molecules like IRF8 and ID2. Flow cytometry can assess phenotypic changes, and co-immunoprecipitation validates interactions with partners such as JUNB. Co-culture T cell activation assays can evaluate the impact on CD8+ T cell priming. The model supports immuno-oncology, functional genomics, and vaccine adjuvant research. For additional information, please contact Ascent Research.
