The IL11 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Ca Ski human cervical carcinoma cell line, designed to disrupt the IL11 gene. This knockout model provides a loss-of-function tool for investigating IL11-mediated signaling in a relevant HPV16-positive cancer background.
The Ca Ski cell line is an established model of HPV16-positive human cervical epidermoid carcinoma, widely utilized to study human papillomavirus-driven oncogenesis and the molecular mechanisms of cervical cancer progression. These cells exhibit characteristics of squamous cell carcinoma and retain key signaling pathways relevant to tumor biology, including those mediating cytokine responses and cellular transformation.
IL11 encodes a pleiotropic cytokine belonging to the GP130 cytokine family, which signals through a receptor complex composed of IL11RA and the co-receptor IL6ST (gp130). Ligand binding triggers phosphorylation of JAK1 and JAK2, subsequently activating STAT3, which translocates to the nucleus to regulate transcription of target genes such as MYC, CCND1, BCL2, COL1A1, and MMP9. The pathway is modulated by negative feedback through SOCS3 and is induced by upstream stimuli including TGFB1, oncostatin M, IL1B, prostaglandin E2, and hypoxia. Through this JAK/STAT3 axis, IL11 promotes cell proliferation, survival, migration, and extracellular matrix remodeling, contributing to fibrosis and tumor progression.
In the context of HPV16-positive cervical carcinoma, IL11 signaling has been implicated in promoting tumor cell proliferation, invasiveness, and resistance to apoptosis, thereby facilitating disease progression. Disruption of IL11 in Ca Ski cells provides a physiologically relevant system to dissect its contribution to cervical cancer phenotypes, including epithelial?Cmesenchymal transition, stemness, and chemoresistance, within a defined genetic background driven by HPV oncoproteins.
These knockout cells are suitable for a variety of downstream applications, including analysis of IL11-dependent transcriptional programs by RNA-seq, assessment of JAK/STAT3 pathway activation via phospho-STAT3 immunoblotting, and functional studies using proliferation (MTS/MTT), migration, and invasion assays. They also enable high-throughput screening for IL11 pathway inhibitors and investigation of cytokine crosstalk in the tumor microenvironment. For further technical information and batch-specific quality control data, please contact Ascent Research.
