The CBR4 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatocellular carcinoma line, engineered for loss-of-function studies of the CBR4 gene. This polyclonal format retains cellular heterogeneity inherent to the parental line, offering a robust model for investigating CBR4-mediated processes in liver cancer biology without clonal artefacts.
The SK-HEP-1 cell line, isolated from ascites of a patient with liver adenocarcinoma, displays a hybrid endothelial?Cmesenchymal phenotype characteristic of an aggressive HCC subtype. Widely applied in hepatic drug metabolism and oxidative stress research, SK-HEP-1 provides a relevant background for examining the mitochondrial functions of CBR4, particularly given its intact xenobiotic metabolism pathways and sensitivity to redox perturbations.
CBR4 encodes a mitochondrial carbonyl reductase that catalyzes NADPH-dependent reduction of diverse carbonyl substrates, including toxic quinones and lipid peroxidation products, thereby protecting cells from oxidative damage and preserving mitochondrial lipid homeostasis. Transcription of CBR4 is governed by PPAR??, NRF2, and HNF4??, linking its expression to fatty acid oxidation, antioxidant defense, and liver-enriched regulatory networks. Downstream, CBR4 generates reduced quinone metabolites and attenuates lipid peroxide accumulation, while physically interacting with mitochondrial respiratory chain complexes and utilizing NADPH as a cofactor. Disruption of CBR4 is anticipated to heighten reactive oxygen species levels, alter lipid profiles, and impair mitochondrial metabolic fidelity.
In the SK-HEP-1 context, CBR4 knockout illuminates oxidative stress vulnerabilities and metabolic dependencies relevant to hepatocellular carcinoma progression. The loss of this reductase may enhance sensitivity to ferroptosis inducers, exacerbate steatosis-like lipid accumulation, and reveal compensatory NADPH-generating routes, making this model valuable for studying non-alcoholic fatty liver disease?Cassociated HCC and drug resistance. The parental line??s endothelial/mesenchymal features further enable examination of CBR4??s role in tumor invasiveness and stroma?Ctumor interactions.
This cell product supports a variety of experimental approaches, including western blotting and RT-qPCR for knockout verification, ROS quantification via cell-permeable probes, and lipid accumulation analysis by Oil Red O staining. Additional applications encompass cell viability assays under oxidative challenge (e.g., menadione treatment) and metabolic flux profiling to assess NADPH consumption. These studies facilitate investigations into hepatic drug metabolism, oxidative stress signaling, and metabolic reprogramming in liver cancer. For further information, please contact Ascent Research.
