Cat. No. ARG0203
The Gpx4 Knockout CT26 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse colorectal carcinoma CT26 model. It features constitutive disruption of the GPX4 gene, which encodes a phospholipid hydroperoxidase that protects cells from ferroptosis by reducing lipid peroxides using glutathione. Major regulators include NFE2L2 and TP53, with downstream interactions involving ACSL4, ALOX15, and the GSH synthesis pathway. Applications include characterizing ferroptosis mechanisms, testing small-molecule modulators (e.g., RSL3, erastin), measuring lipid peroxidation and glutathione levels, and performing syngeneic tumor studies in BALB/c mice. It is suited for colorectal cancer research and ferroptosis-targeted therapy development.
| Host Cell | CT26 |
| Gene Name | Gpx4 |
| Gene Identifier | NCBI Gene ID 625249 |
| Temperature | 37°C |
| Atmosphere | 5% CO₂ |
| Sterility testing | Daily monitoring confirms that the cells are free from bacterial, yeast, and fungal contamination. |
| Mycoplasma testing | Negative for mycoplasma through PCR analysis |
| Pathogens | Cells tested negative for HIV-1, HBV, and HCV. |
Intended Use: This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.
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This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.
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.
