The GPR75 Knockout TE1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population generated from the TE1 human esophageal squamous cell carcinoma cell line. This engineered pool features targeted disruption of the GPR75 gene, producing a genetically diverse loss-of-function model that circumvents the bottlenecks of single?cell cloning. Researchers can employ this system to interrogate the contributions of the orphan GPCR GPR75 to metabolic signaling and cancer cell physiology.
The TE1 cell line originates from a primary human esophageal squamous cell carcinoma and serves as an established model for this aggressive malignancy. These adherent epithelial cells retain key oncogenic features, including dysregulated proliferation and metabolic reprogramming, and are widely utilized to study cancer cell signaling and therapeutic vulnerability. The TE1 background thus provides a clinically relevant context for investigating the interplay between GPR75?driven pathways and esophageal tumor biology.
GPR75 encodes an orphan GPCR that couples with G??s, G??i, and G??q heterotrimeric G proteins and interacts with ???arrestins. It predominantly signals through the cAMP/PKA axis, activating the transcription factor CREB, which drives expression of lipogenic targets such as FASN and SCD1. Additionally, GPR75 intersects with insulin signaling components IRS and AKT, linking it to broader metabolic control. In the knockout cells, loss of GPR75 is predicted to dampen cAMP?PKA?CREB signaling, reduce FASN and SCD1 levels, and impair lipid synthesis, providing a system to dissect GPCR?mediated metabolic rewiring in cancer.
In esophageal squamous cell carcinoma, lipid metabolism supports tumor growth and survival, yet the role of orphan GPCRs like GPR75 remains poorly understood. This polyclonal TE1 knockout model enables direct assessment of GPR75??s influence on cancer cell lipogenesis and energy homeostasis. Given the receptor??s implication in systemic metabolic disorders??obesity and type 2 diabetes??these cells facilitate exploration of connections between metabolic syndrome and esophageal malignancy. The model is valuable for translational studies examining how altered GPR75 signaling impacts tumor metabolic dependencies.
These cells support a range of assays: western blot and RT?qPCR confirm GPR75 ablation; cAMP assays and Seahorse metabolic flux analysis evaluate signaling and bioenergetics; oil red O staining visualizes lipid droplets; and RNA?seq reveals transcriptomic changes. Functional studies on proliferation and insulin response further define GPR75??s role. The model is suited for target validation in obesity, diabetes, and cancer contexts. For additional information, please contact Ascent Research.
