The CBR3 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBR3 gene in HGC-27 human gastric adenocarcinoma cells. These cells serve as a loss-of-function model for investigating carbonyl reductase 3 (CBR3) functions. The polyclonal format minimizes clonal artifacts and represents a robust tool for dissecting CBR3-mediated processes in drug metabolism and oxidative stress response. This engineered pool facilitates consistent and reproducible interrogation of CBR3-dependent pathways.
HGC-27 is a metastatic gastric adenocarcinoma cell line derived from a lymph node metastasis of a gastric cancer patient. This aggressively growing cell line is widely used to model gastric carcinoma biology, including metastatic dissemination and drug resistance. Its clinically relevant genetic background makes it particularly suitable for studying molecular mechanisms underlying chemoresistance and tumor progression.
CBR3 encodes an NADPH-dependent carbonyl reductase that reduces carbonyl-containing substrates, including doxorubicin and lipid peroxidation-derived aldehydes. Transcriptional activation by NRF2 and AhR couples CBR3 expression to oxidative stress. The enzyme utilizes NADPH to generate doxorubicinol, a less toxic metabolite, and participates in prostaglandin metabolism by converting prostaglandin H2 to prostaglandin E2. Potential interaction with CBR1 may fine-tune substrate specificity. Through these activities, CBR3 modulates chemosensitivity, redox balance, and inflammatory signaling networks.
In HGC-27 cells, CBR3 is implicated in intrinsic and acquired resistance to carbonyl-containing chemotherapeutics such as anthracyclines. Disruption of CBR3 in this polyclonal knockout model is expected to impair drug detoxification and antioxidant defenses, leading to elevated reactive oxygen species and enhanced doxorubicin cytotoxicity. This model thus permits mechanistic dissection of CBR3??s contribution to gastric cancer chemoresistance and the identification of targetable vulnerabilities linked to altered carbonyl metabolism.
This product is ideal for exploring anthracycline resistance mechanisms, oxidative stress biology, and CBR3 as a therapeutic target in gastric cancer. Experimental approaches include cell viability and apoptosis assays with doxorubicin, ROS quantification, Western blotting and RT-qPCR for expression analysis, and NADPH-dependent enzyme activity measurements. The polyclonal cells are also amenable to high-throughput screening for modulators of CBR3 function. For additional information, contact Ascent Research.
