The JAG1 knockout KYSE-150 polyclonal cells are a CRISPR/Cas9-edited polyclonal human cell population designed to disrupt expression of the JAG1 gene, encoding the Notch ligand Jagged1. This knockout model provides a powerful tool for investigating Notch signaling in an esophageal cancer background. The polyclonal format preserves genetic heterogeneity, enabling robust functional studies without clonal artifacts and allowing assessment of population-level responses to loss of Jagged1.
The host cell line, KYSE-150, was established from a poorly differentiated human esophageal squamous cell carcinoma and carries a p53 mutation, reflecting a clinically relevant genetic background. This cell line serves as a widely used in vitro model for esophageal cancer biology, exhibiting characteristic features such as rapid proliferation, invasive potential, and altered differentiation programs. The p53-mutant status further mimics the genetic instability observed in many advanced esophageal tumors, making these knockout cells particularly suitable for studying oncogenic signaling networks.
Jagged1, encoded by JAG1, is a critical transmembrane ligand for Notch receptors (NOTCH1?C4) that mediates cell-cell communication. Upon ligand-receptor engagement, sequential proteolytic processing by ADAM10 or ADAM17 and the ??-secretase complex releases the Notch intracellular domain (NICD). NICD translocates to the nucleus, where it forms a transcriptional activation complex with RBPJ and MAML1, driving expression of canonical targets such as HES1, HEY1, MYC, and p21. JAG1 expression is itself regulated by upstream factors including E2F1, TGF-?? signaling, hypoxia, and miR-34a, embedding Jagged1 within a broader network controlling cell fate, proliferation, differentiation, and apoptosis.
In esophageal squamous cell carcinoma (ESCC), JAG1-mediated Notch signaling has been implicated in tumor initiation, progression, and therapy resistance. Overexpression of JAG1 is associated with enhanced proliferation, migration, and epithelial-mesenchymal transition (EMT) in ESCC, while loss-of-function studies have revealed context-dependent tumor-suppressive roles. The JAG1 knockout KYSE-150 cells enable dissection of these dual functions directly in the ESCC context, facilitating investigation of Jagged1-dependent mechanisms governing cancer stemness, metastatic behavior, and drug sensitivity. Moreover, these cells provide a relevant model for exploring therapeutic strategies targeting the Notch pathway in p53-mutant tumors.
Researchers can employ these polyclonal knockout cells in a wide array of assays, including Western blotting and RT-qPCR for target validation, flow cytometry for surface receptor analysis, and functional assays such as Transwell migration/invasion, MTT proliferation, and Annexin V apoptosis assays. Notch reporter luciferase systems and co-culture trans-activation experiments allow direct measurement of pathway activity, while drug sensitivity screens can identify compounds overcoming Jagged1-dependent resistance. This product is thus a versatile resource for elucidating the complex roles of Jagged1 in esophageal cancer and beyond. For further details or technical support, please contact Ascent Research.
