The CAT Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the human catalase (CAT) gene has been disrupted in the DLD-1 colorectal adenocarcinoma cell line. This loss-of-function model impairs the enzymatic decomposition of hydrogen peroxide, providing a genetically defined system to investigate oxidative stress biology without relying on pharmacological inhibition. As a heterogeneous polyclonal pool, these cells maintain genetic diversity within the targeted locus, suitable for experiments where clonal variability is not a requirement.
DLD-1 is a widely characterized adherent epithelial cell line originally derived from the colorectal adenocarcinoma of a male patient. These cells serve as a standard in vitro model for colorectal cancer research, including studies of tumor biology, signal transduction, and epithelial barrier function. Their robust growth and well-documented genomic and transcriptomic profiles make them a reliable platform for gene-editing applications aimed at dissecting molecular pathways relevant to oncogenesis and therapeutic response.
CAT encodes catalase, a homotetrameric heme-containing peroxisomal enzyme that converts hydrogen peroxide (H?O?) into water and oxygen, thereby protecting cells from oxidative damage. Catalase expression is transcriptionally regulated by FOXO3, NRF2, and PPAR?? downstream of PI3K/AKT and MAPK signaling, and is induced by H?O? stimulation. The enzyme interacts with the peroxisomal import receptor PEX5 and functions in concert with a network of antioxidant proteins, including SOD1, SOD2, GPX1, GPX4, and peroxiredoxins, while also modulating redox-sensitive transcription factors such as NF-??B, AP-1, and p53.
Disruption of CAT in DLD-1 cells leads to impaired H?O? scavenging, resulting in elevated intracellular reactive oxygen species (ROS) that can activate oxidative stress responses, alter cell proliferation, and trigger apoptosis. This knockout model therefore captures the redox-dependent signaling axis that is frequently dysregulated in colorectal cancer, where catalase deficiency has been linked to increased genomic instability, altered drug sensitivity, and cellular senescence. The DLD-1 background further enables examination of how oxidative stress intersects with oncogenic pathways unique to colorectal adenocarcinoma.
These polyclonal CAT knockout cells are suitable for a range of functional assays, including measurement of ROS levels using DCFH-DA, assessment of cell viability by MTT/XTT, apoptosis detection via Annexin V/PI staining, and immunoblotting or RT-qPCR for key pathway components such as CAT, NRF2, and KEAP1. Additional applications include colony formation assays, comet assays for DNA damage, and H?O? sensitivity profiling. For further details or to discuss how this product can support your research, please contact Ascent Research.
