The CBR1 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 human colorectal carcinoma cell line. This heterogeneous pool contains cells with targeted gene disruptions in CBR1, creating a loss-of-function model to study carbonyl reductase 1 function in a cancer-relevant context. The polyclonal nature avoids clonal artifacts and allows assessment of gene knockout effects across a diverse population, making it suitable for robust functional analyses.
HCT 116 is an adherent epithelial cell line widely utilized as a colorectal cancer model. It harbors activating mutations in KRAS and PIK3CA while retaining wild-type p53, facilitating studies on oncogenic signaling, DNA damage responses, and drug sensitivity. The well-characterized background supports investigations into tumor proliferation, apoptosis, and metastasis, providing a reliable platform for genetic perturbation.
CBR1 encodes an NADPH-dependent carbonyl reductase that reduces carbonyl groups on endogenous and exogenous substrates. It plays a key role in prostaglandin metabolism by converting prostaglandin E2 to PGF2??, thereby modulating FP receptor-mediated signaling. CBR1 is transcriptionally regulated by NRF2, p53, AhR, and PPAR??, and it interacts with substrates such as 4-hydroxy-2-nonenal, menadione, and the chemotherapeutic daunorubicin. Through these activities, CBR1 influences antioxidant defense, xenobiotic metabolism, and cellular responses to oxidative stress.
In HCT 116 cells, CBR1 knockout likely disrupts PGE2 inactivation, leading to sustained pro-tumorigenic signals that may enhance proliferation and migration. Loss of CBR1-mediated detoxification of reactive aldehydes and quinones could sensitize cells to oxidative stress and alter chemosensitivity. The interplay between CBR1 and p53/NRF2 pathways in this background offers a valuable model for dissecting mechanisms linking redox balance to cancer cell fate.
Researchers can utilize this knockout model for Western blotting and RT-qPCR to confirm gene disruption, PGE2 ELISA to measure prostaglandin levels, MTT assays for proliferation, ROS measurement for oxidative stress, and migration/invasion assays to study metastatic potential. Drug sensitivity assays with substrates like daunorubicin enable chemoresistance studies, while flow cytometry facilitates cell cycle and apoptosis analysis. This product thus supports investigations of colorectal cancer metabolism, prostaglandin signaling, and drug resistance. For further information, please contact Ascent Research.
