The IL1B Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Ca Ski cervical carcinoma line, designed for targeted disruption of the IL1B gene. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells suitable for loss-of-function analysis of the pro-inflammatory cytokine IL-1?? in an epithelial cancer context, avoiding clonal selection bias.
Ca Ski cells are an adherent epithelial line from a metastatic cervical epidermoid carcinoma containing an integrated HPV16 genome. They constitutively express viral oncoproteins E6 and E7, which inactivate p53 and Rb, making them a well-established model for HPV-driven cervical carcinogenesis and therapeutic response studies.
IL1B encodes pro-IL-1??, which is processed by caspase-1 upon inflammasome activation; secreted IL-1?? binds IL-1R1, recruiting MyD88 and activating IRAK4/1 and TRAF6. This triggers TAK1-dependent activation of the IKK complex and MAP kinases (ERK, p38, JNK), leading to NF-??B and AP-1-driven transcription. Upstream regulators include TLR ligands, TNF, IL-1??, and inflammasome activators; downstream targets comprise IL-6, IL-8, PTGS2, and MMPs. Interactions with IL-1R2 and IL-1RA modulate signal strength.
In the HPV16-positive Ca Ski context, IL-1?? links oncogenic transformation to chronic tumor microenvironment inflammation, promoting progression, immune evasion, and therapy resistance. IL1B disruption enables dissection of its role in EMT, angiogenesis, and immunosuppressive cell recruitment, as well as investigation of crosstalk with HPV oncoproteins and inflammatory pathways.
Applications include ELISA for IL-1?? secretion, western blotting of phospho-NF-??B and p-p38, RT-qPCR of IL6 and IL8, proliferation and migration assays, and ASC speck formation for inflammasome activation. This polyclonal knockout model supports studies on drug resistance, immune checkpoint modulation, and tumor-stroma interactions. For inquiries, please contact Ascent Research.
