The CBR1 Knockout NCI-H1299 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBR1 gene in the human NCI-H1299 non-small cell lung cancer cell line. This genetically disrupted cell pool provides a loss-of-function model for investigating the roles of carbonyl reductase 1 in drug metabolism, oxidative stress, and cancer biology. As a polyclonal population, these cells represent a heterogeneous mix of edited alleles, enabling robust functional studies without clonal selection artifacts.
NCI-H1299 is a widely used epithelial-derived cell line established from a lymph node metastasis of a lung adenocarcinoma. It serves as a representative model for non-small cell lung carcinoma metastasis and is extensively employed in cancer research to dissect mechanisms of tumor progression, metastasis, and therapeutic resistance. The host cell background offers a clinically relevant platform for examining how genetic ablation of CBR1 influences lung adenocarcinoma pathophysiology.
Carbonyl reductase 1 (CBR1) is an NADPH-dependent oxidoreductase that catalyzes the reduction of diverse carbonyl substrates, including xenobiotics, quinones, prostaglandins, and anthracycline chemotherapeutics. CBR1 is transcriptionally regulated by NRF2/NFE2L2 and the aryl hydrocarbon receptor (AHR) in response to oxidative stress and xenobiotic exposure. The enzyme functionally interacts with NADPH and substrate quinones, and its activity modulates downstream effectors such as reduced quinone intermediates, prostaglandin F2??, and reactive oxygen species (ROS) levels. Representative pathway components frequently co-analyzed with CBR1 include NQO1, AKR1C1, PTGS2, and various cytochrome P450 enzymes, highlighting its integration within drug metabolism and redox regulatory networks.
In the NCI-H1299 lung adenocarcinoma metastatic model, disruption of CBR1 is predicted to alter cellular sensitivity to anthracycline agents, such as doxorubicin, and to modify responses to oxidative insults. This knockout polyclonal cell product thus provides a defined system to dissect CBR1-mediated drug detoxification pathways and to evaluate how loss of this reductase reshapes the metabolic and signaling landscape of lung cancer cells. It is particularly suited for probing mechanisms of acquired chemoresistance and for identifying compensatory pathways that may become activated upon CBR1 ablation.
Key research applications include cancer drug resistance studies using standardized drug sensitivity assays, redox biology investigations employing ROS detection kits, and metabolism-focused chemotherapeutic assessments. The polyclonal cells are compatible with standard validation techniques, such as Western blotting for CBR1 protein levels and carbonyl reductase activity assays, as well as transcriptomic analyses via RNA-seq to map pathway alterations. These cells also support lung cancer model development, including co-culture and in vivo xenograft studies, to explore tumor-microenvironment interactions. For further technical specifications, protocol recommendations, or to discuss experimental customization, please contact Ascent Research.
