The CAT Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with targeted disruption of the catalase (CAT) gene in human HGC-27 gastric carcinoma cells. This polyclonal format provides a heterogeneous knockout pool, ideal for loss-of-function studies without the bias of single-cell cloning, and serves as a robust tool for researching catalase-related cellular functions.
HGC-27, derived from a metastatic gastric adenocarcinoma of a Japanese patient, is an established epithelial cell line widely used in gastric cancer research. It retains key oncogenic properties, including tumorigenicity in vivo, and is a standard model for studying gastric tumor cell biology and therapeutic responses.
Catalase (CAT) is a primary antioxidant enzyme that decomposes hydrogen peroxide to water and oxygen, protecting cells from oxidative damage. Its expression is regulated by transcription factors such as FOXO3a, Nrf2, NF-??B, and PPAR??, acting through PI3K/AKT and MAPK pathways. CAT activity controls H?O? levels, thereby influencing HIF-1?? stabilization, AP-1 activation, and caspase-mediated apoptosis. CAT functionally interacts with superoxide dismutase (SOD), glutathione peroxidase, NADPH oxidase, and peroxins (PEX5, PEX7) within the broader Nrf2-KEAP1-peroxiredoxin network. CRISPR/Cas9-mediated CAT disruption impairs H?O? detoxification, elevating ROS and potentially promoting oxidative DNA damage and redox-sensitive signaling alterations.
In the context of HGC-27 gastric adenocarcinoma, CAT knockout intensifies the endogenous oxidative stress characteristic of gastric cancer cells, providing a physiologically relevant system to explore redox imbalance in tumor progression. This model is instrumental for studying catalase-dependent drug resistance mechanisms and for evaluating pro-oxidant therapeutic strategies. It also enables dissection of crosstalk between catalase and other antioxidant pathways, such as the glutathione and thioredoxin systems, under disease-relevant conditions.
Key applications include monitoring ROS levels via DCFDA fluorescence, assessing oxidative DNA damage with the comet assay, and evaluating cell viability and apoptosis responses to oxidative or chemotherapeutic stress. Western blotting and catalase activity assays verify gene disruption, while RT-qPCR detects changes in downstream targets like HIF-1?? and Nrf2. These polyclonal knockout cells support investigations of redox signaling, antioxidant defense, and tumorigenic mechanisms in gastric cancer. For further details, please contact Ascent Research.
