The DPP7 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which DPP7 (dipeptidyl peptidase 7) gene disruption abolishes the lysosomal serine protease activity, providing a versatile loss-of-function model for exploring DPP7-dependent cellular processes. Derived from the SK-HEP-1 liver adenocarcinoma cell line, this polyclonal pool offers a biologically relevant system while preserving the heterogeneity typical of tumor cell populations, obviating the need for single-cell cloning and avoiding clonal artifacts.
SK-HEP-1 is a well-established cell line originally isolated from the ascites of a patient with liver adenocarcinoma. It displays a unique mixture of epithelial and endothelial characteristics, making it a valuable model for hepatic cancer studies and endothelial-like functions. The cell line is widely employed to investigate tumor cell apoptosis, angiogenic properties, and cancer immunology, providing a robust platform for functional genomics in the context of hepatocellular carcinoma.
DPP7 encodes a lysosomal serine protease that cleaves dipeptides with a penultimate proline residue, with well-characterized roles in apoptosis and antigen presentation. In the intrinsic apoptotic cascade, DPP7 proteolytically processes BID to generate tBID, which then engages BAX to promote mitochondrial cytochrome c release, leading to activation of caspase-9 and caspase-3. This proteolytic step is regulated by apoptotic stimuli and inflammatory cytokines such as TNF and IFNG. Additionally, DPP7 contributes to the generation of MHC class I antigenic peptides for immune surveillance. The knockout thus disrupts both BID/tBID-mediated mitochondrial death signaling and immune peptide processing, highlighting its multifunctional impact.
In the SK-HEP-1 background, DPP7 knockout provides a powerful tool to dissect apoptosis resistance mechanisms frequently observed in liver adenocarcinoma. Because SK-HEP-1 cells co-express endothelial markers, the model also permits investigation of how loss of DPP7-dependent proteolysis affects endothelial-like behaviors, such as vascular mimicry or angiogenic signaling, in a tumor context. Furthermore, the dual impairment of apoptosis and antigen presentation pathways makes this polyclonal knockout population particularly relevant for studying immune evasion and therapy response in hepatic malignancies.
Researchers can utilize the DPP7 Knockout SK-HEP-1 Polyclonal Cells in a wide range of experimental contexts, including apoptosis research, cancer biology, and immunology. Representative assays include Western blotting for BID cleavage and caspase activity, flow cytometric detection of annexin V/PI staining and MHC class I surface expression, dipeptidyl peptidase activity measurements, qPCR analysis of apoptotic genes, and cell proliferation assays. The polyclonal model is also suitable for drug screening aimed at identifying protease inhibitors or combinatorial treatments that restore cell death or immune recognition in liver cancer. For additional technical information or lot-specific data, please contact Ascent Research.
