The CBR1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the MES-OV human ovarian endometrioid carcinoma cell line. This heterogeneous ensemble of cells harbors targeted disruption of the CBR1 gene, providing a physiologically relevant loss-of-function model that avoids the artifacts of clonal selection. The polyclonal format is ideally suited for robust functional genomics studies, drug screening campaigns, and signaling pathway dissections where population-level responses are critical.
The MES-OV cell line is derived from a human ovarian endometrioid carcinoma, a distinct histological subtype of epithelial ovarian cancer. These cells retain key features of the original tumor, including hormone receptor expression and specific signaling dependencies, making them a valuable tool for investigating ovarian cancer pathogenesis, metastatic progression, and therapeutic resistance. Their use as a host background enables direct relevance to endometrioid carcinoma research.
CBR1 encodes an NADPH-dependent carbonyl reductase that catalyzes the reduction of diverse carbonyl substrates??including prostaglandins, steroid hormones, and xenobiotics??thereby controlling inflammatory signaling, oxidative stress responses, and cellular detoxification. Its expression is transcriptionally regulated by NRF2, aryl hydrocarbon receptor (AhR), PPAR??, and estrogen receptor. Functionally, CBR1 decreases prostaglandin E2 (PGE2) while increasing prostaglandin F2?? (PGF2??), reduces reactive carbonyl species, and alters steroid hormone metabolite profiles. The enzyme requires NADPH as a cofactor and interacts with NRH:quinone oxidoreductase 2 (NQO2) and aldo-keto reductase family members to coordinate cellular redox balance.
In the MES-ovarian cancer context, CBR1 disruption is pivotal for dissecting mechanisms of chemoresistance and tumor progression. CBR1-driven prostaglandin switching and carbonyl detoxification can influence cell proliferation, apoptosis, and migration. Loss of CBR1 sensitizes cancer cells to oxidative stress and may reverse resistance to chemotherapeutic agents such as cisplatin and doxorubicin. This model thus allows researchers to interrogate the intersection of lipid mediator metabolism and redox homeostasis in ovarian endometrioid carcinoma.
This polyclonal knockout product supports a comprehensive suite of applications, including drug sensitivity profiling via MTT/XTT assays; quantification of PGE2 levels by ELISA; reactive oxygen species detection; Western blot and RT-qPCR for target validation; apoptosis assessment with Annexin V/PI; migration analysis using scratch wound or transwell assays; carbonyl reductase enzymatic activity measurement; and transcriptome-wide expression profiling by RNA-seq. These cells facilitate investigations into ovarian cancer drug resistance, prostaglandin-dependent signaling, NRF2?CAhR pathway biology, and biomarker discovery. For further information, please contact Ascent Research.
