CAT Knockout NCI-H1975 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population from the NCI-H1975 human lung adenocarcinoma line, with disrupted catalase (CAT) gene function. The heterogeneous polyclonal format avoids clonal selection bias and supports loss-of-function studies of catalase in a cancer-relevant context, enabling investigation of oxidative stress responses and redox signaling.
NCI-H1975 is a non-small cell lung adenocarcinoma epithelial line harboring EGFR L858R/T790M mutations and a TP53 mutation, derived from a female patient. This well-characterized model exhibits sensitivity and acquired resistance to EGFR tyrosine kinase inhibitors and reflects advanced lung cancer genetics, making it valuable for studying oncogenic signaling, drug resistance, and redox biology.
Catalase is a peroxisomal enzyme that decomposes hydrogen peroxide into water and oxygen, protecting cells from oxidative stress. Its expression is regulated by FOXO3a and NFE2L2 downstream of AKT and KEAP1, and by PPARG. By reducing intracellular H2O2, catalase inhibits NF-??B and MAPK pathway activation and prevents oxidative DNA damage. It cooperates with superoxide dismutase (SOD1/2) and glutathione peroxidase (GPX1), and its peroxisomal localization relies on PEX5 and PEX7 receptors. Catalase thus serves as a critical modulator of redox-sensitive signaling and cell survival.
In NCI-H1975 cells, catalase knockout likely enhances sensitivity to oxidative stress, unmasking vulnerabilities in redox regulation. The EGFR mutant background may exacerbate ROS accumulation, and catalase deficiency could alter drug responses and apoptotic thresholds. This polyclonal model enables dissection of how antioxidant defenses intersect with oncogenic mutations to influence lung adenocarcinoma cell behavior.
Applications include catalase activity assays, H2O2 measurement, ROS detection with DCFH-DA, western blotting, RT-qPCR for oxidative stress markers, immunofluorescence for peroxisomes, cell viability under H2O2 treatment, comet assay, and flow cytometry for apoptosis. These cells support research into oxidative stress in lung cancer, drug resistance, redox biology, tumor microenvironment, and screening of catalase modulators. Contact Ascent Research for technical inquiries.
