The CBR4 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited human gastric cancer cell population in which the CBR4 gene has been disrupted to create a heterogeneous knockout model. This polyclonal product avoids the selection pressures of single-cell cloning, providing a gene-disrupted pool that reflects greater genetic diversity. The population is suitable for bulk functional assays, pooled CRISPR screens, and studies requiring a representative mix of knockout variants within the HGC-27 background.
The host cell line, HGC-27, is an epithelial human gastric cancer line originally derived from a lymph node metastasis of a poorly differentiated gastric adenocarcinoma. These cells are extensively characterized and widely employed to investigate the molecular mechanisms underlying gastric cancer progression, metastasis, and drug resistance. Their metastatic origin makes them particularly relevant for examining aggressive tumor biology.
CBR4 is an NADPH-dependent carbonyl reductase that catalyzes the reduction of diverse endogenous and xenobiotic carbonyl substrates, including reactive aldehydes and ketones. The enzyme functions downstream of oxidative stress signals, regulated by the transcription factor NRF2 and responsive to reactive oxygen species (ROS). NADPH acts as an essential cofactor for the reduction reaction, generating detoxified alcohol products. By intercepting electrophilic carbonyls, CBR4 maintains redox homeostasis and limits damage to proteins, lipids, and nucleic acids.
In the HGC-27 context, disruption of CBR4 expression eliminates this detoxification node, potentially leading to accumulation of cytotoxic carbonyls and elevated ROS levels. As cancer cells already operate under heightened oxidative stress, the loss of CBR4 may impair proliferation and survival, while also enhancing sensitivity to chemotherapeutic agents or oxidative insults. This knockout model thus enables dissection of the carbonyl reduction pathway??s contribution to gastric cancer cell fitness and its role in redox adaptation.
Key applications include cell viability assays (MTT/CCK-8), apoptosis quantification, ROS detection, metabolic profiling, and drug sensitivity screening to assess the functional consequences of CBR4 loss. Expression analysis by RT-qPCR and Western blotting validates knockout efficiency and downstream pathway modulation. The polyclonal nature also facilitates pooled genetic screening for synthetic lethal interactions. For further details, please contact Ascent Research.
