The JAG1 Knockout Ca Ski Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the Ca Ski human cervical squamous cell carcinoma line, carrying a targeted disruption of the JAG1 gene. This knockout model provides a loss-of-function system for studying JAG1-dependent processes without the assumption of monoclonality or homozygosity, preserving natural heterogeneity of the edited pool. The polyclonal format is well-suited for bulk functional assays and high-throughput screening approaches where complete gene ablation may not be required.
The parental Ca Ski cell line is an adherent epithelial line established from an epidermoid carcinoma metastasis of the cervix. It is HPV16-positive with integrated viral genome, representing a classic model for epithelial transformation and HPV-driven oncogenesis. Ca Ski cells exhibit robust proliferative and invasive properties, making them an ideal host for examining the contribution of specific genes to cervical cancer pathogenesis and therapeutic resistance.
JAG1 encodes a canonical Notch ligand that mediates cell?Ccell communication by interacting with NOTCH1, NOTCH2, and NOTCH3 receptors. Upon receptor engagement, ADAM17 and gamma-secretase complexes cleave NOTCH, releasing the NICD intracellular domain, which translocates to the nucleus and binds RBPJ and MAML1 to activate transcription of target genes including HES1, HEY1, MYC, CCND1, BCL2, SNAI1, and SLUG. Upstream regulators such as TGF-beta, TNF-alpha, and HIF1A (under hypoxia) induce JAG1 expression, while downstream effectors drive proliferation, survival, and epithelial-mesenchymal transition. In cervical cancer, JAG1?CNOTCH signaling has been implicated in promoting EMT via SNAI1 upregulation, leading to enhanced invasion and chemoresistance.
In the Ca Ski background, JAG1 disruption allows dissection of its context-dependent roles as a tumor promoter or suppressor. Given the cell line’s HPV16-positive status and origin from metastatic carcinoma, this model is particularly relevant for studying how JAG1 influences invasive behavior, cisplatin sensitivity, and stemness features in a cervical cancer setting. The polyclonal knockout population enables assessment of pathway inhibition effects across a mixed genetic background, closely mimicking therapeutic intervention scenarios.
Researchers can employ these cells to investigate JAG1-mediated Notch signaling, EMT, and drug resistance via functional assays such as transwell migration/invasion, MTT proliferation, caspase-3/7 apoptosis, and cisplatin sensitivity tests. Standard molecular analyses include western blotting for JAG1, HES1, and cleaved NOTCH1; RT-qPCR for HES1, MYC, and SNAI1; and flow cytometry for NOTCH1 surface expression. The knockout model also supports transcriptome profiling by RNA-seq and screening for Notch pathway inhibitors. For further technical details or custom requests, please contact Ascent Research.
