The IL3 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Ca Ski human cervical carcinoma cell line, featuring disruption of the IL3 gene. This product provides a loss-of-function tool for investigating interleukin-3 (IL-3) biology in an epithelial tumor context. The polyclonal nature ensures representation of diverse editing events, suitable for functional studies where clonal averaging is desired.
Ca Ski is an HPV-16-positive cervical epidermoid carcinoma cell line, widely used in cervical cancer research for studies on oncogenesis, drug response, and tumor microenvironment interactions. Its epithelial adherent phenotype and well-characterized genome make it a robust host for CRISPR-based genetic modifications.
IL-3 is a hematopoietic growth factor that stimulates proliferation and differentiation of multipotent progenitors and activates basophils and mast cells. It can also modulate the tumor microenvironment. IL-3 signals through a heterodimeric receptor composed of IL3RA and CSF2RB, activating JAK2. This leads to phosphorylation of STAT5, which regulates gene expression, and recruitment of Shc, Grb2, and SOS, triggering the MAPK/ERK cascade and PI3K/AKT pathway. Downstream effectors include ERK1/2, AKT, the survival protein Bcl-xL (BCL2L1), and the proliferation driver c-Myc. Transcriptional control of IL3 involves NFAT, AP-1, and NF-??B, and is induced by stimuli such as T cell receptor activation, IL-2, IL-18, or PMA/ionomycin.
Knocking out IL3 in Ca Ski cells eliminates IL-3 production, abrogating autocrine/paracrine signaling through the IL-3 receptor. This is particularly relevant for dissecting IL-3’s role in an HPV-positive cervical carcinoma background, potentially revealing non-canonical functions in epithelial cell survival, proliferation, migration, or cytokine secretion. The model enables clean investigation of IL-3R-mediated signaling without background cytokine expression.
This knockout model supports diverse applications, including studies of IL-3 signaling in cervical cancer, tumor-immune crosstalk, and drug screening for IL-3R-targeted agents. As an isogenic control for IL-3 overexpression experiments, it provides a defined genetic background. Typical assay readouts include RT-qPCR for IL3 mRNA, ELISA for IL-3 protein, Western blot for phospho-STAT5, phospho-ERK1/2, and phospho-AKT, cell proliferation and apoptosis assays, flow cytometry for IL3RA and CSF2RB, RNA-seq, cytokine bead arrays, and migration assays. For further technical inquiries, please contact Ascent Research.
