The JAG1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human tongue squamous cell carcinoma epithelial cell line, with targeted disruption of the JAG1 gene. This polyclonal pool enables functional loss-of-function studies of Jagged-1 in a heterogeneous background that mimics tumor heterogeneity, without clonal isolation. It is suitable for dissecting JAG1-dependent Notch signaling in oral cancer research.
The CAL-27 parental line was established from a tongue squamous cell carcinoma of a 56-year-old male patient and is a widely used oral cancer model. These adherent epithelial cells retain invasive properties and dysregulated signaling networks, endogenously expressing Notch receptors and pathway components, making them an appropriate system to study JAG1-mediated cell-cell communication in squamous cell carcinoma.
JAG1 encodes Jagged-1, a transmembrane ligand that directly activates Notch receptors (NOTCH1, NOTCH2, NOTCH3) upon cell-cell contact. Ligand engagement induces ADAM17-mediated ectodomain shedding and ??-secretase cleavage, liberating the Notch intracellular domain (NICD). NICD translocates to the nucleus, associates with the transcription factor RBP-J/CSL and Mastermind-like (MAML) coactivators, and promotes transcription of HES1, HEY1, MYC, and CCND1 target genes. JAG1 expression is regulated by upstream factors such as TGFB1, WNT3A, HIF1??, and inflammatory cytokines (IL-1??, TNF-??), and is modulated by the E3 ligase MIB1. Through this signaling axis, Jagged-1 influences cell fate determination, proliferation, and apoptosis, with crosstalk to Wnt and TGF-?? pathways.
In oral SCC, JAG1 likely promotes tumor progression, invasion, and stemness by sustaining Notch activity. Dysregulated JAG1 has been linked to epithelial-mesenchymal transition, tumor-stroma crosstalk, and drug resistance. This knockout model allows dissection of its specific contributions to NICD nuclear signaling, target gene activation, and tumor microenvironment modulation, while also enabling exploration of pathway redundancy and compensatory mechanisms.
Key applications include studying Notch signaling in oral SCC, tumor-stroma interactions, drug resistance, cancer stem cell biology, and target validation. The cells are compatible with Western blot (JAG1, NOTCH1, NICD, HES1), RT-qPCR, Notch reporter assays, migration/invasion and proliferation assays, xenograft models, co-IP, immunofluorescence, flow cytometry, and RNA-seq. For further information, contact Ascent Research.
