The CCS Knockout HGC-27 Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCS gene has been disrupted via CRISPR/Cas9-mediated gene editing. This polyclonal pool provides a heterogeneous loss-of-function model that allows researchers to study the effects of CCS ablation without the clonal selection artifacts that can arise from single-cell?Cderived knockout lines. The product is supplied as a ready-to-use polyclonal cell population, suitable for immediate expansion and downstream applications.
The HGC-27 host cell line is a well-characterized human gastric carcinoma epithelial cell line originally derived from a metastatic lymph node of a gastric carcinoma patient. This cell line is widely employed in cancer biology research to investigate the molecular mechanisms governing gastric adenocarcinoma proliferation, metastasis, and drug resistance. As an adherent epithelial line, HGC-27 retains key features of gastric tumor biology, making it a relevant model system for exploring tumor cell signaling and therapeutic vulnerabilities.
CCS (Copper Chaperone for Superoxide Dismutase) encodes a copper chaperone that is essential for the delivery of copper ions to superoxide dismutase 1 (SOD1), a critical antioxidant enzyme. CCS binds copper ions and physically interacts with SOD1 to facilitate copper incorporation, which is required for SOD1 enzymatic activation. Once activated, SOD1 catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide, thereby attenuating oxidative stress. The CCS-SOD1 axis operates within a broader copper homeostasis network that includes ATOX1, the copper transporters ATP7A and CTR1, and is regulated by copper ion availability, the metal-responsive transcription factor MTF1, and the transcription factor SP1. This pathway is central to antioxidant defense and is conserved in Homo sapiens.
Disruption of CCS in the HGC-27 gastric carcinoma background creates a powerful model to interrogate the intersection between copper metabolism and cancer cell redox biology. Because HGC-27 cells are known for their aggressive phenotype and relevance to metastasis and drug resistance studies, loss of CCS is expected to impair SOD1 activation, leading to diminished antioxidant capacity and elevated reactive oxygen species (ROS) levels. This perturbation can unmask dependencies on copper homeostasis and oxidative stress responses that support gastric cancer cell survival, proliferation, and chemoresistance. Consequently, the CCS knockout model serves as a valuable tool for dissecting the role of copper chaperone activity in tumor biology and for evaluating the therapeutic potential of targeting copper-related pathways.
This polyclonal knockout cell product is ideally suited for a range of research applications, including investigations of copper chaperone function, oxidative stress response mechanisms, and cancer cell vulnerability under altered redox conditions. Researchers can employ these cells in superoxide dismutase activity assays, ROS detection using probes such as DCFDA, copper uptake and efflux measurements, and immunoblotting for CCS and SOD1 protein levels. Additionally, they facilitate drug sensitivity screening and viability assays under oxidative challenge, with relevance to both gastric cancer biology and neurodegenerative disease research, given the link between CCS and amyotrophic lateral sclerosis. For further details, please contact Ascent Research.
