The CASP4 Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the CASP4 gene has been disrupted. This pooled format provides a loss-of-function model suitable for functional genomic studies without requiring single-cell cloning. The polyclonal knockout cells enable researchers to investigate the role of CASP4 in non-canonical inflammasome signaling and inflammatory cell death pathways.
The A2780 host cell line is a human ovarian adenocarcinoma epithelial cell line originally established from an untreated patient. These cells serve as a well-characterized tumorigenic model for ovarian cancer, exhibiting properties of epithelial ovarian carcinoma and frequently employed in oncology and signal transduction research. The A2780 background is particularly valuable for exploring interactions between inflammatory signaling and ovarian cancer biology.
CASP4 (caspase-4) is an inflammatory caspase that functions as an intracellular sensor for lipopolysaccharide (LPS). Upon recognition of cytoplasmic LPS, CASP4 undergoes activation and directly cleaves gasdermin D (GSDMD), triggering pyroptosis??a lytic form of programmed cell death that releases interleukin-1?? (IL-1??) and interleukin-18 (IL-18). CASP4 is regulated by upstream signals including interferon-gamma (IFN-??), Toll-like receptor 4 (TLR4) signaling, and guanylate-binding proteins (GBPs), and it feeds into the NLRP3 inflammasome pathway via ASC and caspase-1 to amplify inflammatory responses.
In the A2780 ovarian cancer context, disruption of CASP4 impairs non-canonical inflammasome activation, leading to dampened pyroptosis and reduced release of pro-inflammatory cytokines. This knockout model is therefore essential for dissecting how ovarian carcinoma cells cope with intracellular pathogens and inflammatory stress, and for elucidating the contribution of CASP4 to the tumor microenvironment. The loss of CASP4 may alter the cells?? sensitivity to LPS and other inflammatory stimuli, providing insights into immune evasion mechanisms in ovarian cancer.
This knockout cell population is ideal for a wide range of experimental applications, including the study of pyroptosis and inflammasome biology, investigation of LPS-induced signaling pathways in ovarian cancer, and screening for small-molecule inhibitors of pyroptosis. Compatible assays include western blotting, RT-qPCR, LDH release assays, IL-1?? ELISA, propidium iodide uptake, GSDMD immunofluorescence, caspase activity measurements, and transcriptomic profiling by RNA-seq. For additional technical details and ordering information, please contact Ascent Research.