HCAR2 Knockout TE1 Polyclonal Cells are a heterogeneous population of human esophageal squamous cell carcinoma cells engineered to disrupt the HCAR2 gene through CRISPR/Cas9-mediated gene editing. This polyclonal knockout model introduces loss-of-function mutations across the target locus, generating a diverse set of edited alleles ideal for studying HCAR2-dependent signaling in a cancer-relevant background. The product provides a versatile tool for investigating receptor-mediated metabolic and anti-inflammatory pathways without the constraints of single-clone variability.
The TE1 cell line, derived from a human esophageal squamous cell carcinoma, exhibits an epithelial morphology and is widely employed as a model for upper aerodigestive tract malignancies. These adherent cells retain key signaling networks characteristic of squamous carcinomas, making them suitable for examining the interplay between oncogenic pathways and metabolic regulator receptors. The HCAR2 knockout in TE1 cells permits dissection of receptor function within a malignant epithelial context, complementing studies in normal or immune cell types.
HCAR2, a G protein-coupled receptor activated by niacin, butyrate, and ??-hydroxybutyrate, couples primarily to the Gi family of G proteins. Ligand binding triggers Gi-mediated inhibition of adenylyl cyclase, decreasing intracellular cAMP levels, which attenuates protein kinase A activity and suppresses lipolysis in adipocytes. Downstream, HCAR2 signaling promotes phosphorylation of ERK1/2 and inhibits NF-??B, contributing to anti-inflammatory effects. The receptor also interacts with ??-arrestin and GPCR kinases (GRKs), which regulate receptor desensitization and trafficking. Representative pathway components include sequential engagement of HCAR2, Gi, adenylyl cyclase, cAMP, and PKA, leading to reduced lipolysis, and parallel activation of the MAPK/ERK cascade.
In the context of esophageal squamous cell carcinoma, HCAR2 may modulate tumor cell behavior through its anti-inflammatory and metabolic signaling arms. Loss of HCAR2 function could alter lipid metabolism, cytokine responses, and MAPK pathway dynamics, influencing proliferation, migration, or apoptosis. This knockout model enables researchers to explore HCAR2??s role in cancer metabolism and its potential as a therapeutic target in malignancies where metabolic reprogramming and inflammation converge.
This HCAR2 knockout polyclonal cell population is suitable for pharmacological studies of niacin receptor agonists, dissection of Gi-coupled GPCR signaling, and functional assays related to anti-lipolytic and anti-inflammatory mechanisms. Researchers can evaluate receptor-mediated cAMP modulation, ERK phosphorylation, lipid accumulation, and transcriptional responses via RT-qPCR and western blotting. Additional applications include migration/invasion assays, apoptosis profiling, and drug sensitivity screening in the context of dyslipidemia, colitis, or atherosclerosis research. For further technical details and ordering information, please contact Ascent Research.
