The GGCT Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human Raji B lymphocytes. This heterogeneous pool with targeted disruption of the GGCT gene, encoding gamma-glutamylcyclotransferase, provides a loss-of-function model free from clonal artifacts. The CRISPR/Cas9-mediated gene disruption enables investigation of GGCT??s role in glutathione metabolism and redox regulation.
The Raji cell line originates from a Burkitt lymphoma patient, exhibiting MYC oncogene overexpression due to chromosomal translocation. As suspension B lymphocytes, Raji cells are widely used in immunology and oncology, especially for humoral immunity and antibody production studies. Their robust proliferation and well-characterized pathways make them ideal for gene editing. The Raji background is clinically relevant for studying GGCT in MYC-driven B-cell lymphomas and oxidative stress.
GGCT encodes gamma-glutamylcyclotransferase, which converts gamma-glutamyl dipeptides to 5-oxoproline and free amino acids, linking amino acid transport to glutathione metabolism. This reaction is crucial for maintaining glutathione, an antioxidant composed of glutamate, cysteine, and glycine. Transcriptionally regulated by NRF2 and c-Myc in response to oxidative stress and oncogenic signals, GGCT cooperates with gamma-glutamyl transpeptidase to process gamma-glutamylcysteine and with glutamate-cysteine ligase to channel cysteine into glutathione synthesis. Its disruption impairs 5-oxoproline production, altering glutathione synthesis and redox-sensitive signaling, thereby connecting GGCT to antioxidant defense and metabolic control.
In Raji cells, MYC overexpression imposes high metabolic and oxidative demands. GGCT knockout disrupts redox balance by reducing 5-oxoproline levels and compromising glutathione recycling, sensitizing cells to oxidative stress and agents like cisplatin and hydrogen peroxide. The polyclonal nature captures heterogeneous knockout effects across the cell population, enabling study of GGCT-dependent vulnerabilities in B-cell lymphomas without clonal selection bias. Impairing the gamma-glutamyl cycle, this model highlights therapeutic targets in glutathione metabolism for MYC-driven cancers and other malignancies such as breast, gastric, and lung carcinomas.
These polyclonal knockout cells support glutathione metabolism research (GSH/GSSG ratio measurement), cancer redox biology (ROS detection), and drug target validation (sensitivity to oxidative stress-inducing compounds). Assays include western blotting for GGCT, RT-qPCR, cell proliferation and apoptosis flow cytometry, and metabolomics profiling of gamma-glutamyl cycle intermediates such as 5-oxoproline. The model enables oxidative stress response studies and GGCT signaling exploration in Burkitt lymphoma. For further details, contact Ascent Research.
