The CASP7 Knockout SK-HEP-1 Polyclonal Cells from Ascent Research consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CASP7 gene in the human SK-HEP-1 hepatic adenocarcinoma cell line. As a polyclonal pool, this product retains the natural heterogeneity of the parental cells, providing a robust loss-of-function model for studying caspase-7 biology without the artifacts associated with monoclonal selection. The gene editing was achieved through CRISPR/Cas9-mediated gene disruption, generating a mixed population of edited cells suitable for population-level assays in apoptosis research.
The SK-HEP-1 host cell line was originally derived from the ascitic fluid of a patient with hepatic adenocarcinoma and is a widely used model of hepatocellular carcinoma. This cell line exhibits characteristic features of malignant liver cells, including aberrant regulation of apoptotic pathways and inherent chemoresistance mechanisms. Consequently, SK-HEP-1 cells provide a physiologically relevant background for investigating the functional role of caspase-7 in liver cancer cell survival and death signaling.
Caspase-7, encoded by CASP7, functions as an executioner caspase that is proteolytically activated by initiator caspases such as CASP8, CASP9, and CASP10, as well as by granzyme B. Once activated, caspase-7 cleaves multiple downstream substrates, including PARP1, DFFA, LMNA, ACTB, GAS2, and ROCK1, driving the biochemical and morphological hallmarks of apoptosis. Its activity is tightly controlled by interactions with the inhibitor XIAP and the activator SMAC/DIABLO, and it can form both homodimers and heterodimers with caspase-3 (CASP3). The BCL2 family members BAX and BCL2 indirectly regulate caspase-7 activation by modulating mitochondrial cytochrome c (CYCS) release, which triggers the APAF1-dependent activation of CASP9.
In the SK-HEP-1 hepatic adenocarcinoma model, where apoptosis is frequently dysregulated, this CASP7 knockout population enables precise investigation of caspase-7??s contribution to cell death induction and chemosensitivity. By eliminating executioner caspase activity, researchers can dissect the relative importance of caspase-7 versus caspase-3 in mediating apoptosis triggered by intrinsic and extrinsic stimuli. This model is particularly useful for studying how liver cancer cells may evade apoptosis through reduced caspase-7 expression or activity, and for identifying compensatory survival mechanisms that arise in the absence of this executioner protease.
The CASP7 Knockout SK-HEP-1 Polyclonal Cells are ideally suited for a wide range of functional studies, including apoptosis resistance assays, chemosensitivity screening, and drug target validation. Representative experimental readouts include Western blotting for cleaved caspase-7 and its substrates, Annexin V apoptosis assays, caspase-3/7 luminescent activity measurements, and cell viability assays such as MTT or CCK-8. Immunofluorescence and flow cytometry-based methods can further quantify active caspase-7 levels and apoptotic cell populations. Additionally, these cells enable the study of inflammatory caspase signaling cross-talk and the evaluation of therapeutic agents that exploit caspase-dependent cell death pathways. For additional details, please contact Ascent Research.
