The JAG2 Knockout CAL-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the CAL-27 human tongue squamous cell carcinoma line, designed for loss-of-function studies of the JAG2 gene. This polyclonal knockout model disrupts JAG2 expression through CRISPR/Cas9-mediated gene targeting, generating a heterogeneous pool of edited alleles that collectively ablate JAG2 function without clonal selection. The product is supplied as a ready-to-use cell population, enabling researchers to investigate the multifaceted roles of JAG2 in oral squamous cell carcinoma biology.
The parental CAL-27 cell line originates from a primary, moderately differentiated squamous cell carcinoma of the tongue and exhibits adherent epithelial morphology. Widely used as an HNSCC model, CAL-27 retains active Notch, PI3K/AKT, and MAPK/ERK pathways, making it a relevant system for dissecting JAG2-dependent mechanisms in tumor progression, metastasis, and therapeutic resistance.
JAG2 encodes a transmembrane ligand for Notch receptors (NOTCH1?C4) and mediates juxtacrine cell?Ccell communication. Upon ligand-receptor interaction, ADAM10/ADAM17-mediated cleavage triggers gamma-secretase-dependent release of the Notch intracellular domain (NICD). NICD translocates to the nucleus and forms a transcriptional complex with CSL (RBP-J??) and coactivator MAML1 to induce expression of target genes such as HES1, HEY1, MYC, CCND1, SNAI1, and ZEB1. This signaling axis is modulated by EGFR, TGF-??, NF-??B, AP-1, and intersects with PI3K/AKT and MAPK/ERK cascades, forming a regulatory network that governs cell proliferation, survival, and epithelial-mesenchymal transition (EMT).
In CAL-27 cells, JAG2-driven Notch activation supports oncogenic phenotypes, contributing to enhanced proliferation, apoptosis resistance, and acquisition of invasive and stem-like properties. By eliminating JAG2 function in a polyclonal context, this knockout model permits assessment of both cell-autonomous and non-cell-autonomous effects within a heterogeneous tumor cell population, closely mimicking the clonal diversity of clinical tumors. Consequently, it provides a robust platform for examining how JAG2 loss influences CAL-27 behavior in standard in vitro assays and in vivo xenograft models, and for validating JAG2 as a candidate therapeutic target in HNSCC.
Typical applications include functional characterization of JAG2 via western blotting, RT-qPCR, proliferation, migration, and invasion assays, as well as flow cytometry for Notch surface expression. The polyclonal format is particularly suited for co-culture systems with Notch reporter lines or stromal cells to dissect ligand-dependent signaling dynamics. Moreover, these cells can be employed in xenograft tumor models to evaluate metastatic potential and drug responses in the absence of JAG2. For more information or to discuss custom applications, please contact Ascent Research.
