The IL1R1 Knockout Ca Ski Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the endogenous IL1R1 gene. This product provides a heterogeneous pool of cells harboring gene disruptions, offering a robust loss-of-function model without requiring single-cell cloning. The polyclonal format facilitates rapid deployment in functional studies by preserving cellular diversity while ablating IL-1 receptor type 1 expression. Genome editing is achieved through CRISPR/Cas9-mediated gene editing, generating a versatile tool for interrogating IL1R1-dependent signaling in a human cervical cancer context.
The host cell line, Ca Ski, is an adherent epithelial cell line derived from a metastatic cervical squamous cell carcinoma of the small intestine. It stably harbors integrated HPV16 genome, making it a well-characterized model for studying HPV-positive cervical carcinogenesis. The cells retain key features of the original malignancy, including metastatic origin and responsiveness to inflammatory stimuli. This background provides a clinically relevant platform for investigating the interplay between viral oncogenesis and host inflammatory pathways.
IL1R1 encodes the primary receptor for interleukin-1 cytokines, binding IL-1?? (IL1A) and IL-1?? (IL1B), with regulatory antagonism by IL-1RA (IL1RN). Upon ligand engagement, IL1R1 heterodimerizes with the co-receptor IL1RAP, which recruits the adaptor proteins MYD88 and IRAK4, activating IRAK1 and the E3 ubiquitin ligase TRAF6. This complex orchestrates downstream activation of the IKK complex and MAP kinase cascades, leading to nuclear translocation of NF-??B and induction of transcription factors JUN and FOS. Key downstream effector genes include IL6, CXCL8, and PTGS2, which amplify pro-inflammatory signals. The pathway interfaces with Toll-like receptor and NOD-like receptor signaling, and negative regulators such as TOLLIP modulate signal strength.
In Ca Ski cells, IL1R1-mediated signaling is implicated in promoting inflammation-driven tumor progression, including enhanced proliferation, invasion, and immune modulation. HPV16 oncoproteins E6 and E6 may synergize with IL-1 signals to exacerbate malignant phenotypes, making this knockout model particularly valuable for dissecting receptor-specific contributions to cervical cancer pathology. The polyclonal nature avoids clonal artifacts, enabling unbiased assessment of IL1R1 function in a genetically relevant metastatic cervical cancer environment.
This product supports diverse research applications: functional analysis of IL-1 signaling in cervical cancer, drug screening for IL-1R antagonists, and study of inflammation-induced metastasis. Representative assays include western blotting and RT-qPCR for confirming gene disruption and downstream target expression, ELISA-based quantification of secreted IL-6 and CXCL8 following IL-1?? stimulation, NF-??B luciferase reporter assays, and migration or invasion assays to evaluate metastatic capacity. Co-immunoprecipitation can be employed to investigate receptor?Cadaptor interactions. For further technical guidance or customized applications, please contact Ascent Research.
