The GPR75 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the HGC-27 human gastric adenocarcinoma cell line. This heterogeneous pool of cells harbors targeted disruptions in GPR75, enabling loss-of-function studies in a cancer-relevant background. The polyclonal population preserves genetic diversity while ensuring robust target-gene knockout, suitable for bulk-population assays where clonal variation is not a priority.
HGC-27 is a human gastric adenocarcinoma cell line derived from a metastatic lymph node of a gastric carcinoma patient. Exhibiting an undifferentiated, epithelial morphology, it serves as a widely used model in oncology for studying tumor biology, drug response, and signaling pathways. Its origin makes it particularly relevant for investigating molecular mechanisms of gastric cancer progression and evaluating therapeutic interventions.
GPR75 is a Gq/11-coupled receptor that binds 20-hydroxyeicosatetraenoic acid (20-HETE), a bioactive lipid mediator derived from arachidonic acid metabolism. Upon activation, GPR75 engages G??q/11 to stimulate phospholipase C?? (PLC??), which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers calcium release from the endoplasmic reticulum, while DAG activates protein kinase C (PKC), leading to the phosphorylation of downstream effectors including the MAPK/ERK pathway. The receptor also interacts with ??-arrestin-1 and ??-arrestin-2, which modulate receptor desensitization and G-protein-independent signaling. Upstream, the production of 20-HETE is mediated by cytochrome P450 enzymes such as CYP4A11 and CYP4F2. Through this signaling cascade, GPR75 influences intracellular calcium dynamics and downstream transcriptional programs involved in cell proliferation, migration, and metabolic regulation.
Disruption of GPR75 in HGC-27 cells provides a tool to dissect the 20-HETE/GPR75 axis in gastric adenocarcinoma. GPR75 signaling converges on calcium mobilization and PKC activation, pathways often dysregulated in cancer, thus this knockout model helps assess GPR75’s contribution to cancer cell phenotypes. The gastric cancer background is relevant as aberrant arachidonic acid metabolism and GPCR signaling are implicated in tumor growth, invasion, and metabolic reprogramming. Eliminating GPR75 expression allows investigation of its oncogenic role and identification of therapeutic targets.
This polyclonal knockout cell pool is suitable for functional assays including RT-qPCR and western blotting for expression analysis, calcium flux assays for signaling, and cell proliferation, migration, and colony formation assays for phenotypic characterization. It enables GPCR signal transduction studies, small-molecule screening targeting 20-HETE/GPR75, and obesity research when combined with appropriate stimuli. The polyclonal nature ensures robust, reproducible results in bulk-assay formats. For further information, please contact Ascent Research.
