The ART1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human oral squamous cell carcinoma line CAL-27, engineered to disrupt the ART1 gene. ART1 encodes an arginine-specific ADP-ribosyltransferase that catalyzes NAD+-dependent protein modification. This polyclonal product provides a loss-of-function model for studying ART1-mediated signaling in oral cancer without clonal bias. It circumvents the need for single-cell cloning while preserving genetic diversity, making it suitable for population-level analyses of gene function and therapeutic response.
CAL-27 is an adherent epithelial cell line derived from a primary tongue squamous cell carcinoma of a 56-year-old male, and it serves as a widely used model of OSCC. These cells display hallmarks of aggressive HNSCC, including EGFR and NF-??B pathway activation and EMT plasticity. Their established molecular profile enables rigorous assessment of ART1-dependent oncogenic signaling. The knockout cells generated from this background allow dissection of ART1??s specific contribution to oral cancer pathophysiology in a clinically relevant setting.
ART1 is a GPI-anchored enzyme that ADP-ribosylates cell surface proteins, particularly integrin ??7 (ITGA7), upon binding NAD+. This modification activates PI3K/AKT and NF-??B cascades, upregulating EMT transcription factors (SNAI1) and mesenchymal markers (VIM, MMP2/9), thereby enhancing migration and invasion. ART1 expression is induced by TNF-??, IL-6, and EGF via NF-??B and STAT3. Interacting with RSPO2 and EGFR further amplifies oncogenic signals. Knockout of ART1 is anticipated to disrupt these pro-metastatic circuits, attenuate AKT and RELA phosphorylation, and restore sensitivity to cisplatin.
In the CAL-27 OSCC model, ART1 knockout is valuable for dissecting EMT and integrin-mediated adhesion remodeling. Eliminating ART1 function allows researchers to test the dependency of PI3K/AKT and NF-??B pathways on ART1 activity, measure changes in invasion-related proteins, and evaluate the ART1?CITGA7?CRSPO2 axis. This model also aids in identifying novel ART1 substrates and validating ART1 as a therapeutic target in HNSCC, potentially uncovering strategies to overcome chemoresistance.
Typical applications include mechanistic studies of ADP-ribosylation-dependent metastasis, EMT regulation, and substrate identification. Key assays supported: RT-qPCR and western blotting for EMT markers, Transwell migration/invasion, phospho-specific ELISA, apoptosis and cisplatin sensitivity assays, co-immunoprecipitation (ART1?CITGA7), and flow cytometry. This polyclonal knockout population is essential for academic and pharmaceutical laboratories focusing on HNSCC biology and anti-metastatic drug discovery. For further information, please contact Ascent Research.
