The CASP7 Knockout AGS Polyclonal Cells product comprises a population of genetically modified AGS human gastric adenocarcinoma cells carrying CRISPR/Cas9-mediated disruption of the CASP7 gene, encoding caspase-7. As a polyclonal knockout pool, this product provides a cellular model with heterogeneous gene-disruption alleles, suitable for studying loss-of-function phenotypes in a non-clonal population context.
The AGS host cell line is a widely used model of human gastric adenocarcinoma derived from a primary tumor. These epithelial cells exhibit adherent growth and retain molecular features relevant to gastric carcinogenesis, including dysregulated apoptosis and proliferation signaling pathways. The AGS background provides a context for investigating CASP7 function in gastric cancer biology, particularly in processes such as chemoresistance and tumor cell survival.
CASP7 encodes caspase-7, an executioner caspase that functions downstream of initiator caspases such as caspase-8 and caspase-9 within the apoptotic cascade. Upon proteolytic activation, caspase-7 cleaves a spectrum of cellular substrates including PARP1, DFF45/ICAD, Lamin A/C, and ROCK1, leading to the biochemical and morphological hallmarks of apoptosis. Beyond classical apoptosis, caspase-7 also participates in pyroptotic and inflammatory pathways, processing pro-IL-1?? under inflammasome activation conditions. Its activity is tightly regulated by interactions with XIAP and Survivin, which inhibit caspase-7, and by molecular chaperones such as Hsp70 and the apoptosome component Apaf-1. Upstream signaling inputs include death-receptor pathways mediated by Fas and TRAIL, the intrinsic mitochondrial pathway involving cytochrome c and Apaf-1, and granzyme B delivered by cytotoxic lymphocytes, all converging on activation by caspase-8 or caspase-9.
Disruption of CASP7 in AGS cells is predicted to impair the execution phase of apoptosis, potentially conferring resistance to chemotherapeutic agents that induce apoptotic cell death. Given the role of caspase-7 in pyroptosis and pro-IL-1?? maturation, this knockout model also enables interrogation of inflammatory cell death mechanisms in the context of gastric adenocarcinoma. Consequently, the CASP7 knockout AGS polyclonal cells serve as a valuable tool for dissecting the contributions of caspase-7 to treatment resistance and tumor-associated inflammation.
Researchers can employ this knockout model in a range of downstream assays including Western blotting for caspase-7 and its cleaved substrates, caspase-7 activity measurements, Annexin V/PI flow cytometry for apoptosis quantification, and PARP cleavage analysis. Functional studies such as proliferation and colony formation assays, along with cytokine release profiling and transcriptomic analysis via RNA-seq, facilitate comprehensive assessment of CASP7 loss in gastric cancer cells. These approaches make the CASP7 knockout AGS polyclonal cells suitable for applications spanning apoptosis signaling studies, investigation of drug resistance in gastric cancer, high-content drug screening, and functional genomics. For additional product details or technical support, contact Ascent Research.
