The CBR3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, engineered to disrupt the CBR3 gene encoding carbonyl reductase 3. This polyclonal format provides a heterogeneous pool of cells harboring CRISPR-mediated gene disruptions, enabling the study of CBR3 loss-of-function in a cancer cell background.
HeLa cells are an immortalized human cervical adenocarcinoma epithelial cell line, originally isolated from Henrietta Lacks in 1951. They exhibit an aneuploid karyotype, harbor HPV18 viral sequences, and display robust proliferation, making them a widely utilized model in cancer biology, drug screening, and cell signaling research. Their epithelial origin and well-characterized molecular landscape render them suitable for exploring the impact of CBR3 knockout on carcinoma cell physiology.
CBR3 encodes an NADPH-dependent oxidoreductase that catalyzes the reduction of diverse carbonyl substrates, including endogenous quinones, prostaglandins, and xenobiotic compounds. Within the arachidonic acid metabolism pathway, CBR3 converts prostaglandin E2 to prostaglandin F2??, while in xenobiotic metabolism it detoxifies reactive aldehydes and ketones. Transcription of CBR3 is regulated by stress-responsive factors such as Nrf2 (NFE2L2), the pregnane X receptor (PXR/NR1I2), and the aryl hydrocarbon receptor (AhR). Upon activation, these regulators upregulate CBR3 to enhance cellular defense against oxidative and chemical stress. CBR3 functions in concert with cofactors like NADPH and interacts with substrate quinones; it may also functionally cooperate with the related carbonyl reductase CBR1. Thus, CBR3 sits at the intersection of detoxification, prostaglandin signaling, and steroid hormone biosynthesis pathways, modulating the levels of key metabolites and influencing redox balance.
Disruption of CBR3 in HeLa cells creates a loss-of-function model to dissect the enzyme??s contributions to drug metabolism and stress responses in a cervical adenocarcinoma context. Given HeLa cells?? transformed nature and active proliferation, the knockout is predicted to sensitize cells to oxidative stress and alter the metabolism of carbonyl-containing therapeutic agents, such as anthracyclines. This model enables researchers to probe how carbonyl reductase activity affects cancer cell survival and drug resistance, and to explore the interplay between prostaglandin signaling and epithelial tumor biology.
The CBR3 Knockout HeLa Polyclonal Cells are suited for a variety of investigative applications. They can be employed in cell viability assays under oxidative challenge or drug treatment, Western blotting and RT-qPCR to confirm CBR3 disruption and assess downstream pathway alterations, and LC-MS-based measurement of prostaglandin metabolite shifts. NADPH oxidation assays and drug sensitivity studies with anthracyclines offer functional readouts of carbonyl reductase activity. Researchers can utilize this model to study Nrf2-mediated stress responses, AhR-driven xenobiotic metabolism, and PXR-regulated drug clearance pathways. For further technical details or to request a quote, please contact Ascent Research.
