The CBR3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal cell population designed to disrupt the CBR3 gene, which encodes an NADPH-dependent carbonyl reductase. This polyclonal knockout pool provides a loss-of-function model to investigate the roles of CBR3 in cellular detoxification and oxidative stress response. The heterogeneous population is generated by CRISPR/Cas9-mediated target-gene disruption, offering researchers a versatile tool for studying gene function without single-cell cloning artifacts.
These cells are engineered in the A2780 host cell line, a human ovarian carcinoma line derived from an untreated patient with ovarian endometrioid adenocarcinoma. A2780 serves as a widely used model for high-grade serous ovarian carcinoma, retaining key genetic and phenotypic features of aggressive ovarian cancer. The line??s origin and tumorigenic properties make it particularly suitable for oncological research, including drug resistance and tumor metabolism studies.
CBR3 functions as an NADPH-dependent oxidoreductase that catalyzes the reduction of carbonyl-containing xenobiotics and endogenous reactive carbonyl species, thereby attenuating oxidative damage. The enzyme is transcriptionally regulated by NRF2 (NFE2L2) in response to oxidative stress and electrophilic compounds, acting downstream of the KEAP1-ARE signaling axis. CBR3 interacts with NADPH as a cofactor and cooperates with other phase II detoxifying enzymes such as NQO1 and CYP450 isoforms. Its activity promotes the detoxification of reactive aldehydes and ketones, protecting cells from lipid peroxidation and oxidative stress.
In the A2780 ovarian cancer background, CBR3 knockout is predicted to impair the cell??s ability to reduce and inactivate carbonyl-containing substrates, including certain chemotherapeutic agents. This disruption may increase the accumulation of reactive oxygen species and enhance sensitivity to drugs that undergo carbonyl reduction, such as doxorubicin. Consequently, this model is instrumental for dissecting mechanisms of drug resistance in ovarian cancer, where altered expression of detoxification enzymes can impact therapeutic outcomes. The polyclonal nature of the knockout population minimizes clonal bias while enabling robust functional genomic studies.
Typical applications include investigating drug resistance mechanisms in ovarian cancer, assessing oxidative stress responses, studying chemotherapy metabolism, and performing functional genomics of carbonyl reductases. Researchers can employ Western blotting to confirm CBR3 protein depletion and monitor NRF2 pathway components, RT-qPCR for transcript analysis, ROS detection assays to measure oxidative stress, and MTT-based viability assays with carbonyl-containing drugs like doxorubicin. Genomic PCR serves for knockout confirmation. For additional information or custom requests, please contact Ascent Research.
