The Gpx4 Knockout CT26 Cell Line is a CRISPR/Cas9-edited knockout cell line based on the murine colorectal carcinoma epithelial cell line CT26. This product provides targeted disruption of the Gpx4 gene, encoding glutathione peroxidase 4 (GPX4), a key suppressor of ferroptosis. Loss of GPX4 function enables precise investigation of lipid peroxidation, oxidative stress, and regulated cell death signaling. The line serves as a validated loss-of-function model for studying ferroptosis biology in a tumor-relevant context.
The parental CT26 line was chemically induced in a BALB/c mouse and is characterized as an undifferentiated colon carcinoma with epithelial features. CT26 is a widely used syngeneic model for colorectal cancer, allowing orthotopic or subcutaneous tumor formation in immunocompetent hosts. Its epithelial origin and tumorigenic capacity make it a robust system for studying mechanisms of colon cancer progression and therapeutic response.
GPX4 is a phospholipid hydroperoxidase that reduces lipid hydroperoxides using reduced glutathione (GSH), preventing iron-dependent ferroptotic death. Expression of GPX4 is under transcriptional control of NFE2L2 (NRF2) and is inhibited by TP53, connecting ferroptosis to antioxidant and tumor suppressor pathways. Selenium incorporation via selenoprotein P is required for GPX4 activity. The enzyme counteracts lipid peroxidation driven by ACSL4, LPCAT3, ALOX5, and ALOX15, which oxidize arachidonic acid-containing phospholipids. GPX4 cooperates with SLC7A11-mediated cystine import for GSH synthesis, and operates in parallel with the FSP1/CoQ10 pathway to maintain membrane redox homeostasis.
In the CT26 colon carcinoma context, Gpx4 knockout increases sensitivity to ferroptosis agonists such as RSL3 and erastin, providing a robust model for ferroptosis research. This enables dissection of GPX4-dependent antioxidant defenses in colorectal cancer cells, assessment of ferroptosis vulnerability under metabolic stress, and comparison of ferroptosis sensitivity across tumor subtypes. The model supports exploration of ferroptosis?Capoptosis cross-talk in epithelial malignancies and evaluation of ferroptosis-targeted therapeutic strategies.
This knockout line is suitable for lipid peroxidation detection by C11-BODIPY, cell viability profiling with ferroptosis inducers, glutathione assays, RT-qPCR of ferroptosis markers, and GPX4 Western blotting. In vivo tumorigenesis can be studied via xenograft or syngeneic models in BALB/c mice, linking ferroptosis status to tumor growth. Drug screening applications benefit from the defined ferroptosis sensitivity phenotype. For ordering or technical inquiries, contact Ascent Research.
