The IGF1R Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the CAL-27 human tongue squamous cell carcinoma line. Disruption of the insulin-like growth factor 1 receptor gene yields a heterogeneous loss-of-function model for studying IGF1R-dependent signaling. This product is supplied as live adherent cells for direct experimental use without single-cell cloning.
The CAL-27 host line originates from a metastatic lymph node of an oral squamous cell carcinoma and is HPV-negative with a p53 mutation. Its adherent growth and genetic stability make it a standard platform for oral cancer research. The metastatic origin emphasizes its utility in invasion and progression studies.
IGF1R encodes a receptor tyrosine kinase activated by IGF1, IGF2, and insulin. Ligand binding triggers recruitment of adaptors IRS1 and SHC, initiating the PI3K/AKT/mTOR and GRB2/SOS/RAS/RAF/MEK/ERK cascades. AKT phosphorylates FOXO, GSK3??, and BAD to promote survival and growth, while ERK1/2 drives proliferation. PTEN negatively regulates this axis, and JAK/STAT signaling also receives input from IGF1R.
In CAL-27 cells, IGF1R signaling contributes to the malignant phenotype of head and neck squamous cell carcinoma, a cancer frequently exhibiting IGF1R pathway activation. The HPV-negative, p53-mutant background mirrors a common oral cancer genotype, making this knockout pool a relevant system to dissect IGF1R-mediated oncogenic signals. Ablation of IGF1R eliminates downstream AKT and ERK phosphorylation, offering a clean model to assess pathway dependency.
This product supports diverse applications: western blotting for phospho-AKT and phospho-ERK, RT-qPCR for IGF1R expression, MTT and colony formation assays for viability, Annexin V staining for apoptosis, transwell migration for motility, and drug sensitivity testing with linsitinib to probe resistance mechanisms. Additional readouts include phospho-RTK arrays and cell cycle analysis by flow cytometry. For more information, please contact Ascent Research.
