ELANE Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human CAL-27 oral squamous cell carcinoma line with targeted disruption of the ELANE gene. This product provides a heterogeneous knockout pool, avoiding clonal artifacts and enabling robust loss-of-function analysis of neutrophil elastase (NE) in a cancer cell background. The CRISPR/Cas9-mediated gene disruption eliminates functional ELANE expression, offering a versatile model for studying NE-dependent processes without requiring single-cell clone isolation.
The parental CAL-27 line originates from a human tongue squamous cell carcinoma, harbors a TP53 mutation, and exhibits an invasive, metastatic phenotype. CAL-27 cells grow adherently and are widely employed as a model for aggressive oral cancer, allowing interrogation of apoptosis, migration, and drug response. The TP53-mutant status impairs canonical p53 pathways, providing a tumorigenic context in which ELANE-mediated signaling can be dissected.
ELANE encodes a serine protease that degrades extracellular matrix components like elastin and collagen and promotes caspase-3-mediated apoptosis. Upstream activation by TNF?? and IL-8, and transcriptional regulation by CEBPA, direct ELANE expression. ELANE interacts with SERPINA1, MPO, and PRTN3 to modulate proteolytic activity. Downstream effects include CD4 receptor cleavage and NF??B pathway modulation through TLR engagement. These interactions link ELANE to neutrophil extracellular trap formation, inflammatory signaling, and tumor microenvironment dynamics.
ELANE knockout in CAL-27 cells abrogates NE-mediated apoptosis and matrix degradation, potentially enhancing tumor cell survival and altering inflammatory responses. This model enables investigation of how cancer cells may escape immune-mediated killing by neutrophils and how the tumor microenvironment is remodeled in the absence of NE. It provides a clean cellular background for studying paracrine NE effects or for ectopic expression of ELANE variants associated with congenital neutropenia.
Researchers can apply this knockout model to evaluate apoptosis resistance, migration/invasion capacity, and inflammation-related signaling in TP53-mutant cancers. Compatible assays include Western blotting, RT-qPCR, flow cytometry for CD4 and apoptotic markers, and co-immunoprecipitation of ELANE-associated partners like SERPINA1. Please contact Ascent Research for additional technical details and support.
