The IGF2 Knockout Ca Ski Polyclonal Cells represent a genetically disrupted population of Ca Ski cervical carcinoma cells, engineered via CRISPR/Cas9-mediated gene targeting to ablate expression of the insulin-like growth factor 2 (IGF2) gene. This polyclonal knockout pool provides a heterogeneous loss-of-function model, enabling robust analysis of IGF2-dependent phenotypes in a human cervical cancer background without the introduction of clonal artifacts. The product is supplied as a polyclonal cell population, each carrying a targeted disruption within the IGF2 locus, and is suitable for downstream applications requiring pooled knockout cells.
Ca Ski cells are an adherent epithelial cell line established from a cervical epidermoid carcinoma, and they harbor the integrated human papillomavirus type 16 (HPV-16) genome. This line is widely employed as a model for HPV-mediated oncogenesis, faithfully recapitulating aspects of cervical cancer progression, including deregulated cell cycle control and genomic instability. The epithelial morphology and stable HPV-16 status provide a physiologically relevant context for investigating growth factor signaling, viral-host interactions, and therapeutic interventions.
IGF2 encodes a potent mitogenic and anti-apoptotic growth factor that functions primarily through autocrine and paracrine activation of the insulin-like growth factor 1 receptor (IGF1R). Ligand binding triggers phosphorylation of insulin receptor substrate 1 (IRS1) and SHC adaptor proteins, initiating two major downstream cascades: the PI3K/AKT/mTOR axis and the RAS/RAF/MEK/ERK pathway. These networks converge on key effectors including AKT, ERK1/2, mTOR, Cyclin D1, and MYC, promoting cell cycle progression, protein synthesis, and survival. IGF2 signaling is tightly regulated by upstream factors such as the H19 long noncoding RNA, CCCTC-binding factor (CTCF), and genomic imprinting mechanisms, and it interacts with a network of binding partners, including IGF1R, the insulin receptor, IGF2R, and IGF-binding proteins (IGFBPs). Dysregulation of this pathway is implicated in multiple cancers and growth disorders, notably Beckwith-Wiedemann syndrome and Wilms tumor.
In the context of Ca Ski cells, IGF2 signaling contributes to the transformed phenotype by sustaining proliferation and suppressing apoptosis, likely cooperating with HPV-16 oncoproteins E6 and E7. Disruption of IGF2 in this polyclonal knockout model enables the dissection of its role in cervical tumorigenesis, including effects on cell cycle regulation, metabolic reprogramming, and resistance to chemotherapeutic agents. The model is particularly suited for interrogating the interplay between growth factor signaling and viral oncogenes, as well as identifying synthetic lethal interactions that may inform therapeutic strategies.
Typical research applications include functional characterization of IGF2 in cervical cancer progression, elucidation of HPV-16-driven signaling networks, and drug resistance studies. The knockout cells can be employed in a variety of assays, such as western blotting and RT-qPCR to confirm loss of IGF2 and downstream target modulation, cell proliferation and apoptosis assays to assess growth phenotypes, phospho-signaling analysis to map pathway activity, migration and invasion assays, and RNA sequencing for transcriptome-wide insights. Additionally, these cells are suitable for xenograft tumor models to evaluate tumorigenic potential in vivo. For additional technical details and ordering information, please contact Ascent Research.
