The HCAR2 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population of the HCAR2 (hydroxycarboxylic acid receptor 2) gene in the human KYSE-150 esophageal squamous cell carcinoma cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous cell pool with ablated HCAR2 expression. The polyclonal format captures a spectrum of editing outcomes, enabling functional studies without clonal selection bias and providing a robust tool for interrogating HCAR2 biology in a cancer context.
KYSE-150 is a well-characterized human esophageal squamous cell carcinoma cell line derived from a poorly differentiated tumor. It serves as a widely used in vitro model for esophageal cancer research, retaining malignant features such as rapid proliferation, invasive capacity, and dysregulated signaling networks. The adherent monolayer growth habit and established culture protocols make KYSE-150 cells amenable to standard molecular and cellular biology techniques, facilitating detailed mechanistic investigations.
HCAR2, also known as GPR109A, encodes a Gi/o-coupled receptor activated by endogenous ligands including niacin, butyrate, and ??-hydroxybutyrate. Upon ligand binding, HCAR2 inhibits adenylyl cyclase, lowering intracellular cAMP levels and consequently attenuating protein kinase A (PKA) activity and cAMP response element-binding protein (CREB)-mediated transcription. This signaling cascade further modulates mitogen-activated protein kinase (MAPK) pathways and suppresses nuclear factor-kappa B (NF-??B) activation, underpinning the receptor??s anti-inflammatory and metabolic effects. HCAR2 promotes adiponectin secretion in adipocytes and engages ??-arrestins, enabling G protein-independent signaling branches. By integrating metabolic and inflammatory inputs, HCAR2 orchestrates diverse cellular responses relevant to homeostasis and disease.
In the context of esophageal squamous cell carcinoma, HCAR2 may influence tumor cell behavior through its metabolic and anti-inflammatory functions. KYSE-150 cells exhibit aberrant signaling networks characteristic of aggressive esophageal cancer, and disruption of HCAR2 could alter responses to metabolic stress, lipid mediators, or niche-derived signals. Given the receptor??s capacity to regulate NF-??B and MAPK activity, the knockout model provides a platform to dissect the crosstalk between nutrient sensing and oncogenic pathways, with potential implications for understanding how dietary metabolites or pharmacological HCAR2 modulators affect cancer cell proliferation, survival, and invasive properties.
Research applications for this HCAR2 polyclonal knockout population include GPCR signaling assays (cAMP measurement and ??-arrestin recruitment), Western blotting for downstream effectors such as phosphorylated CREB and MAPKs, RT-qPCR, RNA-sequencing, and phenotypic analyses including migration, invasion, and drug sensitivity testing. The model supports niacin receptor functional studies, metabolic regulation research, anti-inflammatory mechanism investigation, and esophageal cancer drug target validation. The polyclonal nature offers a population-level perspective on gene disruption. For further information, please contact Ascent Research.
