The IL17RB Knockout Ca Ski Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma cell line Ca Ski. This product targets the IL17RB gene, encoding a receptor for IL-17B and IL-25, using CRISPR/Cas9-mediated gene disruption to generate a heterogeneous pool of edited cells. The resulting polyclonal cells offer a loss-of-function model for investigating IL17RB-dependent signaling without clonal isolation.
Ca Ski is an adherent epithelial cell line originating from a cervical epidermoid carcinoma metastasis and carries integrated human papillomavirus type 16 (HPV-16) DNA. As a well-characterized model of HPV-associated cervical cancer, Ca Ski cells endogenously express IL17RB and respond to its ligands, making them suitable for studying IL-17 family cytokine signaling in a cervical cancer context. This polyclonal knockout population retains the parental line’s HPV-16 status and epithelial morphology while lacking functional IL17RB expression across the majority of cells.
IL17RB functions as a receptor for cytokines IL-17B and IL-25 (IL-17E). Ligand binding induces heterodimerization with IL17RA, recruiting the adaptor Act1 (TRAF3IP2) and TRAF6. This complex activates NF-??B and MAP kinase pathways, leading to transcriptional induction of pro-inflammatory genes and Th2-type cytokines. Representative downstream targets include IL-6, IL-8, CXCL1, and CCL20. Through these pathways, IL17RB promotes inflammatory responses, tissue remodeling, and Th2 differentiation. In cervical cancer, IL17RB signaling may contribute to tumor-associated inflammation and metastasis.
In Ca Ski cells, IL17RB knockout abrogates responses to IL-17B and IL-25, providing a tool to dissect receptor function in cervical cancer. Because Ca Ski cells are HPV-16 positive, this model is valuable for examining crosstalk between IL17RB-mediated signaling and viral oncogenes. Disruption of IL17RB may attenuate NF-??B and MAPK activation, potentially reducing secretion of inflammatory mediators that support tumor growth, angiogenesis, and immune evasion. Researchers can use these polyclonal knockout cells to determine whether IL17RB signaling promotes malignant phenotypes such as proliferation, migration, or invasion.
These IL17RB knockout Ca Ski cells enable functional studies, including cytokine response assays measuring changes in gene expression by RT-qPCR or secreted cytokine levels by ELISA. Western blotting and NF-??B reporter assays can assess pathway activation, while proliferation and migration assays evaluate receptor roles in tumor cell behavior. The model supports drug target validation and investigation of IL17RB as a therapeutic target in cervical cancer and inflammatory diseases. Co-immunoprecipitation may probe receptor complex assembly. For further details, please contact Ascent Research.
