The ATP7B Knouckout HGC-27 Polyclonal Cells provide a polyclonal CRISPR/Cas9-edited population of HGC-27 gastric carcinoma cells with targeted disruption of the ATP7B gene. The knockout pool avoids clonal selection biases and supports loss-of-function studies of this copper-transporting ATPase. Gene editing was accomplished via CRISPR/Cas9-mediated gene disruption, generating a heterogeneous collection of edited alleles suitable for robust, population-level analyses.
HGC-27 is a human gastric adenocarcinoma epithelial cell line isolated from a lymph node metastasis, widely used as a model for advanced gastric cancer. Its metastatic origin and cancerous phenotype make it a relevant system to examine genes influencing tumor progression and drug response. This host background enables investigation of ATP7B??s role in copper handling within the context of gastric carcinoma.
ATP7B encodes a P-type ATPase that localizes to the trans-Golgi network and exports copper into secretory pathways or bile. It is a keystone of copper homeostasis, activated by copper ions and regulated by proteins including ATOX1, COMMD1, and MTF-1. ATP7B interacts directly with ATOX1, COMMD1, and the scaffold p62/SQSTM1, and drives synthesis of cuproenzymes such as ceruloplasmin (CP). The pathway integrates ATOX1, COMMD1, CP, MT1, and copper ions to control intracellular copper trafficking and efflux. Disruption of ATP7B by CRISPR/Cas9 abrogates this network, altering copper flux and downstream signaling.
In gastric cancer, copper homeostasis modulates proliferation and redox balance. The ATP7B knockout HGC-27 model permits dissection of how disrupted copper transport impacts tumor cell behavior, including potential effects on MAPK or PI3K pathways. It also serves as a cellular system for studying Wilson disease, an autosomal recessive copper toxicity disorder, and related copper accumulation syndromes, thus linking cancer biology with metal metabolism disorders.
This product enables diverse research applications: copper uptake/efflux measurements, ICP-MS for cellular copper, RT-qPCR of copper-responsive genes, and western blot or immunofluorescence for pathway components. Drug screening with copper-modulating compounds, functional complementation with ATP7B variants, and studies of Wilson disease pathogenesis are facilitated. MTT assays can assess copper sensitivity. For technical details, please contact Ascent Research.
