The CAT Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line, designed for disruption of the CAT gene encoding catalase. This polyclonal product provides a heterogeneous pool of loss-of-function models that collectively eliminate catalase-mediated antioxidant defense, enabling robust investigations into oxidative stress biology.
The 143B cell line is a well-characterized human osteosarcoma model originating from the HOS (human osteosarcoma) derivative, commonly employed in bone cancer research, metastasis studies, and evaluation of cellular responses to therapeutic agents. Its adherent growth, stable karyotype, and defined oncogenic mutations render it a reliable platform for gene-editing applications aimed at interrogating tumor biology.
Catalase is a peroxisomal heme enzyme that decomposes hydrogen peroxide into water and oxygen, forming a critical antioxidant defense. Its expression is transcriptionally activated by Nrf2 (NFE2L2) and modulated by PPAR?? and FoxO factors. Catalase functions downstream of H2O2, interacting with peroxisomal import receptors PEX5 and PEX14 and chaperones. It is a central component of the Nrf2-Keap1 pathway and is linked to PI3K/Akt signaling, thereby lowering intracellular ROS and protecting macromolecules.
In the osteosarcoma context, loss of catalase activity exacerbates oxidative stress, which can have dual consequences??promoting genomic instability and apoptosis while potentially inducing adaptive resistance mechanisms. Given the metabolic peculiarities of bone cancer cells, this knockout model allows dissection of how redox imbalance influences tumor proliferation, invasiveness, and sensitivity to chemotherapeutic agents that rely on ROS generation.
Researchers can employ these cells in catalase activity assays, Amplex Red-based H2O2 measurement, DCFDA ROS detection, western blotting for catalase and oxidative stress markers, and comet assays for DNA damage. Applications include redox-dependent signaling dissection, osteosarcoma drug resistance studies, and evaluation of pro-oxidant therapies. For further technical information, please contact Ascent Research.
