The CAT Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CAT gene in the Ca Ski human cervical carcinoma line. This loss-of-function model disrupts catalase expression, enabling investigation of oxidative stress and redox signaling in an epithelial cancer context. The polyclonal format provides a heterogeneous, yet validated, pool for functional studies without clonal selection.
Ca Ski is an HPV16-positive cervical adenocarcinoma cell line established from a metastatic site. These adherent epithelial cells stably maintain integrated HPV16 genomes and express the E6 and E7 oncoproteins, which inactivate p53 and pRb, respectively. Ca Ski cells are extensively used in cervical cancer research, drug discovery, and viral oncology. Their inherent susceptibility to HPV-induced oxidative stress makes them a relevant model for probing catalase-mediated antioxidant defense.
Catalase is the primary enzyme responsible for detoxifying hydrogen peroxide (H2O2) into water and oxygen, thereby mitigating oxidative damage. Its expression is under the transcriptional control of FOXO3a and NFE2L2/NRF2, which respond to insulin, hypoxia, and redox imbalance. Catalase functions within a network including superoxide dismutases (SOD1, SOD2) that produce H2O2, and glutathione peroxidase 1 (GPX1) and peroxiredoxin 1 (PRDX1) as parallel H2O2 scavengers. Catalase activity requires NADPH as a cofactor and a heme group for catalysis; its peroxisomal localization involves PEX family proteins. Downstream, catalase limits oxidative DNA damage, reduces lipid peroxidation, and suppresses NF-??B activation. The interconnected pathways of SOD1/2, catalase, GPX1, PRDX1, thioredoxin (TXN), and thioredoxin reductase (TXNRD1) collectively preserve cellular redox homeostasis.
In Ca Ski cells, HPV16 oncoprotein-driven ROS production creates a constitutive oxidative burden. CAT knockout is expected to amplify H2O2 accumulation, thereby potentiating oxidative stress, DNA damage, and redox-sensitive signaling such as NF-??B. This altered state may shift cell fate toward apoptosis or alter proliferation dynamics, directly relevant to cervical cancer progression and drug resistance. The model thus provides a unique platform to study how abrogation of a single antioxidant enzyme influences HPV-associated malignancy and response to therapeutic interventions that induce oxidative damage.
These polyclonal knockout cells are suited for catalase activity assays, Amplex Red H2O2 quantification, and western blot analysis of catalase and oxidative stress markers (4-HNE, protein carbonyls). ROS detection by DCFDA, cell viability under H2O2 stress, and Annexin V apoptosis assays enable functional phenotyping. Migration, invasion, and RNA-seq profiling further elucidate catalase’s role. Applications span investigation of redox signaling, chemosensitivity, and HPV-mediated carcinogenesis. For additional product information, researchers may contact Ascent Research.
