The IGF1R Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski human cervical epidermoid carcinoma cell line. This product features targeted disruption of the IGF1R gene, which encodes the insulin-like growth factor 1 receptor, a receptor tyrosine kinase. The polyclonal format provides a heterogeneous pool of gene-edited cells, enabling functional studies where clonal homogeneity is not required. These cells serve as a loss-of-function model for investigating IGF1R-mediated signaling in a cervical cancer context.
The Ca Ski host cell line originated from a human cervical epidermoid carcinoma and is stably integrated with human papillomavirus type 16 (HPV16) sequences. These cells exhibit adherent growth and are widely employed as a model for HPV16-positive cervical cancer. Ca Ski cells retain key epithelial characteristics and express viral oncoproteins E6 and E7, which perturb tumor suppressor pathways. This genetic background makes them particularly relevant for studying the intersection of viral oncogenesis and growth factor signaling.
IGF1R is a transmembrane receptor tyrosine kinase activated by its ligands IGF1 and IGF2, with modulation by insulin and IGF-binding proteins (IGFBPs). Upon ligand engagement, IGF1R undergoes autophosphorylation and recruits insulin receptor substrate 1 (IRS1) and IRS2, as well as the adaptor protein SHC. These events trigger two principal signaling cascades: the PI3K/AKT pathway, involving phosphoinositide 3-kinase (PI3K) and downstream effectors AKT, mTOR, and FOXO transcription factors, and the MAPK/ERK pathway, mediated through GRB2, SOS, RAS, RAF, MEK, and ERK1/2. The negative regulator PTEN antagonizes PI3K signaling. IGF1R activation promotes cell cycle progression via cyclin D1 and suppresses apoptosis through phosphorylation of BAD and regulation of BCL2 family members.
In Ca Ski cells, IGF1R signaling likely cooperates with HPV16 oncoproteins to drive proliferation and survival. Disruption of IGF1R in this polyclonal population impairs IGF1/IGF2-mediated signaling, potentially leading to reduced AKT and ERK phosphorylation, cell cycle arrest, and increased apoptosis. This model allows dissection of how IGF1R contributes to the malignant phenotype of HPV-positive cervical carcinoma, independent of clonal selection biases. It is suitable for evaluating how the loss of IGF1R alters cellular responses to external growth factors and chemotherapeutic agents.
Typical research applications include cancer biology studies focused on cervical cancer, drug target validation, and signaling pathway analysis. Researchers can use these cells to perform Western blotting for phosphorylated AKT (Ser473) and ERK1/2 (Thr202/Tyr204), RT-qPCR for downstream targets such as CCND1 and BCL2, proliferation assays (MTT or BrdU incorporation), apoptosis assays (Annexin V staining), cell cycle analysis, migration and invasion assays, and xenograft tumor growth studies. These applications enable comprehensive functional genomics and pharmacological investigations. For additional technical details or support, please contact Ascent Research.
