The IGF2 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human oral squamous cell carcinoma cell line CAL-27. This product provides a heterogeneous pool of cells harboring gene disruptions at the IGF2 locus, offering a loss-of-function model for investigating insulin-like growth factor II signaling in a tumorigenic epithelial context. The polyclonal format preserves the diversity of edited alleles, enabling robust bulk functional analyses without the clonal selection biases inherent to single-cell-derived lines.
The parental CAL-27 cell line was established from a primary tongue squamous cell carcinoma and is a well-characterized model for oral cancer progression. CAL-27 cells are tumorigenic in nude mice, possess a TP53 missense mutation (R273H), and express epidermal growth factor receptor (EGFR), mirroring key genetic alterations in aggressive oral carcinomas. These features render CAL-27 a relevant host for dissecting growth factor-driven malignant phenotypes.
IGF2 encodes insulin-like growth factor II, a developmentally regulated growth factor frequently overexpressed in oral squamous cell carcinoma and other cancers. IGF2 signals through IGF1R and INSR-A, activating PI3K-AKT and RAS-MAPK/ERK cascades to drive proliferation, survival, and metabolism. Its transcription is regulated by PLAG1, PLAGL2, SP1, E2F1, and imprinting control region methylation. Secreted IGF2 binds IGF1R, INSR-A, the clearance receptor IGF2R, and IGF-binding proteins (IGFBP2, IGFBP3, IGFBP6). Downstream effectors include IRS1, AKT1, mTOR, ERK1/2, and FOXO proteins, leading to Cyclin D1 and BCL2L1 expression.
In the CAL-27 oral cancer model, autocrine or paracrine IGF2 signaling is hypothesized to sustain tumorigenic and invasive traits. Knockout of IGF2 disrupts ligand-dependent activation of IGF1R and INSR-A, thereby attenuating downstream pathways critical for anchorage-independent growth, invasion, and apoptosis resistance. Consequently, the IGF2 Knockout CAL-27 Polyclonal Cells serve as an essential tool for delineating the role of IGF2 in oral cancer progression and for evaluating targeted therapies, including IGF1R inhibitors.
This knockout model supports assays such as western blotting for IGF2 and phospho-AKT/phospho-ERK, RT-qPCR, MTT/BrdU proliferation, Annexin V apoptosis, Transwell migration/invasion, colony formation, and xenograft tumor growth. RNA-seq enables transcriptome-wide analysis. These polyclonal knockout cells facilitate screening of IGF pathway inhibitors and oral cancer mechanistic studies. For further information, contact Ascent Research.
