The CBR4 Knockout A2780 Polyclonal Cells provide a CRISPR/Cas9-engineered polyclonal knockout population of the A2780 human ovarian carcinoma cell line, designed for functional loss of the carbonyl reductase 4 (CBR4) gene. This product consists of a heterogeneous pool of edited cells, delivering a genetically diverse model system that circumvents the phenotypic bias associated with single-cell-derived knockout clones. The polyclonal format enables robust population-level analysis of CBR4-dependent biological processes, making it an ideal starting point for pathway interrogation, drug response profiling, and metabolomic studies in ovarian cancer.
The A2780 cell line, originally established from an untreated ovarian carcinoma patient, exhibits epithelial morphology and is widely used as a model for high-grade serous ovarian cancer research. It retains key oncogenic drivers and metabolic pathways, providing a physiologically relevant background for studying gene function in a disease-relevant context. The cell line??s well-documented growth characteristics and compatibility with standard molecular biology techniques facilitate reproducible experimentation and data integration across studies.
CBR4 encodes an NADPH-dependent carbonyl reductase that reduces carbonyl groups on prostaglandin E2, steroid hormones (estradiol, cortisol), retinoids, and xenobiotics, thereby modulating their bioactivity. The enzyme is centrally positioned in arachidonic acid metabolism, steroid hormone catabolism, and xenobiotic detoxification pathways. Its transcription is regulated by NRF2, PPAR??, PXR (NR1I2), and CAR (NR1I3). CBR4 requires NADPH as a cofactor and may interact with HSP90 and other short-chain dehydrogenases/reductases. Downstream substrates influenced by CBR4 activity include reduced prostaglandin E2, retinoic acid, and reactive carbonyl species; accordingly, knockout is predicted to elevate these metabolites, perturbing signaling through nuclear receptors such as PPAR??, retinoic acid receptors (RAR), retinoid X receptors (RXR), and steroid hormone receptors.
In A2780 cells, CBR4 knockout disrupts carbonyl metabolism, likely accumulating prostaglandin E2 and steroid metabolites that alter tumor phenotypes. Elevated prostaglandin E2 may drive inflammatory and proliferative responses, while altered steroid metabolism could affect estrogen and glucocorticoid receptor signaling, impacting proliferation, migration, and drug sensitivity. The polyclonal knockout model thus offers a robust system for studying drug resistance and metabolic reprogramming, with the population-based design minimizing clonal artifacts.
Applicable to functional assays including cell viability and migration under xenobiotic stress, as well as metabolomic profiling by LC-MS and targeted ELISA for prostaglandin E2. Transcriptomic (RNA-seq, RT-qPCR) and proteomic (Western blot, immunofluorescence) analyses can uncover downstream networks. The cell pool also suits drug screening for carbonyl reductase modulators. For inquiries, contact Ascent Research.
