The JAG2 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by targeted disruption of the JAG2 gene in the KYSE-150 human esophageal squamous cell carcinoma (ESCC) cell line. Comprising a heterogeneous pool of cells with independent JAG2 loss-of-function mutations, this product abolishes Jagged2 protein expression across the population. The polyclonal format preserves the inherent variability of CRISPR-mediated gene editing, providing a physiologically relevant model that mirrors the genetic diversity of tumor cells while avoiding the clonal artifacts of monoclonal knockout lines.
The parental KYSE-150 cell line originates from a poorly differentiated esophageal squamous cell carcinoma resected from a Japanese male patient. These adherent epithelial cells exhibit hallmark features of ESCC, including rapid proliferation, invasive behavior, and dependency on oncogenic signaling cascades. Widely utilized as a preclinical ESCC model, KYSE-150 cells harbor genomic alterations typical of human disease, making them a suitable platform for dissecting gene function in esophageal cancer. The introduction of JAG2 knockout into this background enables precise assessment of Jagged2??s role in ESCC pathogenesis.
JAG2 encodes Jagged2, a type I transmembrane protein that serves as a high-affinity ligand for Notch receptors (NOTCH1?C4). Its expression is transcriptionally governed by E2F1, NFKB1, TGFB1, and HIF1A, integrating signals from proliferation, inflammation, and hypoxia. Upon Notch interaction, Jagged2 triggers a proteolytic cascade involving ADAM17 and ??-secretase, culminating in nuclear translocation of the Notch intracellular domain. NICD complexes with RBPJ and MAML1 to activate target genes such as HES1, HEY1, MYC, and CCND1, which control cell cycle progression, differentiation, and survival. Additionally, LFNG-mediated glycosylation of Notch receptors fine-tunes Jagged2 binding specificity. JAG2-dependent signaling also contributes to epithelial-to-mesenchymal transition and angiogenic programs, processes frequently co-opted during carcinogenesis.
In KYSE-150 ESCC cells, JAG2 knockout eliminates a principal Notch ligand, thereby disrupting downstream transcriptional responses driven by HES1 and MYC. This loss impairs cell proliferation, survival, and migration, key malignant phenotypes in esophageal carcinoma. The polyclonal knockout population captures the spectrum of functional consequences arising from JAG2 disruption, offering a robust system to study Jagged2-specific oncogenic activities without compensation from other Notch ligands. This model is particularly suited for exploring Notch-related mechanisms in ESCC and for validating therapeutic targets within this pathway.
Applications of the JAG2 Knockout KYSE-150 Polyclonal Cells encompass signaling studies, functional genomics, and drug screening. Compatible assays include Western blotting for pathway components, RT-qPCR for target gene quantification, flow cytometry for receptor expression, proliferation assays, and transwell migration tests. The cells enable investigation of ligand-specific Notch functions, evaluation of pharmacological inhibitors, and dissection of feedback loops involving upstream regulators. For additional product details or to request custom modifications, please contact Ascent Research.
