The CHURC1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the human gastric adenocarcinoma AGS cell line. This product offers a heterogeneous loss-of-function model suitable for functional genomics and drug screening without clonal selection bias. The polyclonal format captures population-level phenotypic variability and facilitates robust analysis of CHURC1-dependent processes in a cancer-relevant epithelial background. The product serves as a versatile resource for researchers investigating gene function in gastric adenocarcinoma.
The AGS parental line is a widely used human gastric adenocarcinoma epithelial model, derived from a gastric cancer patient. These cells exhibit gastric epithelial features and are routinely applied in studies of gastric cancer mechanisms, Helicobacter pylori infection, and chemotherapeutic responses. Their consistent in vitro characteristics make them a standard system for investigating proliferative and invasive properties of gastrointestinal cancer cells, and they are frequently employed in drug screening assays.
CHURC1 encodes a transcriptional repressor that integrates signaling from TGF-beta and FGF pathways. It interacts with SMAD2/3 and co-repressors like NCoR/HDACs upon activation by ligands including TGF-beta1, FGF2, and BMP4. CHURC1 represses genes such as NEUROG1, MYC, and CCND1, thereby regulating cell cycle progression and neural differentiation. This repressor also modulates EMT markers, linking its activity to metastatic processes. Key pathway mediators include SMAD4, ERK1/2, and their cognate receptors. Through these interactions, CHURC1 coordinates transcriptional programs that influence cell fate decisions and tumor cell behavior.
In AGS gastric cancer cells, CHURC1 disruption enables dissection of its role in tumor biology, particularly in TGF-beta/FGF-driven proliferation, apoptosis, and EMT. Loss of CHURC1 may alter sensitivity to TGF-beta and FGF inhibitors, providing insights into therapeutic resistance mechanisms. Moreover, given CHURC1’s developmental associations, it allows exploration of how neural programming genes might contribute to oncogenesis in epithelial tissues. This model is thus well-suited for drug target validation and mechanism-of-action studies in a gastric cancer context.
This polyclonal knockout pool supports diverse applications: western blotting and RT-qPCR confirm CHURC1 loss; RNA-seq and ChIP-qPCR profile transcriptomic and genomic occupancy changes; proliferation, migration, and invasion assays quantify functional outcomes; and reporter assays assess TGF-beta/FGF pathway activity. Researchers can combine these approaches to build comprehensive mechanistic models of CHURC1 function in cancer. For detailed protocols or to place an order, please contact Ascent Research.
