The DTX3L Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 liver adenocarcinoma line, designed to disrupt DTX3L gene function. This heterogeneous loss-of-function model avoids clonal selection artifacts and retains the parental line’s diverse genetic background, enabling robust investigation of DTX3L-dependent phenotypes across a mixed allelic pool.
SK-HEP-1 is a widely adopted human hepatocellular carcinoma cell line presenting a mixed endothelial/epithelial phenotype. Originally isolated from ascitic fluid, it serves as a versatile platform for studying liver cancer biology, tumor heterogeneity, and oncogenic signaling, with adherent growth and reliable propagation facilitating genetic manipulation and functional assays.
DTX3L functions as an E3 ubiquitin ligase that modifies target proteins through ubiquitination, influencing their stability and activity. It operates at the nexus of interferon signaling and DNA damage repair: transcriptionally induced by interferon-??/??/?? via STAT1, STAT2, and IRF9, DTX3L interacts with PARP9 and PARP14 to regulate STAT1-driven transcription and NF-??B activation. It also ubiquitinates histone substrates, linking innate immune signaling to chromatin remodeling and stress responses.
In SK-HEP-1 cells, DTX3L disruption provides a pertinent model for dissecting its role in hepatocellular carcinoma. The knockout enables exploration of DTX3L-mediated effects on interferon anti-tumor immunity, DNA repair pathway choice, and NF-??B-dependent survival signals. The mixed phenotype of SK-HEP-1 additionally allows study of DTX3L in tumor cell plasticity and immune evasion, with the polyclonal population mirroring the heterogeneity found in clinical tumors.
This polyclonal knockout pool is suitable for Western blotting and RT-qPCR confirmation of DTX3L ablation; co-immunoprecipitation and ubiquitination assays to examine PARP9 complex formation and substrate modification; immunofluorescence to monitor localization; phospho-STAT1 flow cytometry to assess interferon signaling; and Comet assays or cell viability assays for DNA damage and drug sensitivity studies. For additional details, please contact Ascent Research.
