The IL1R1 Knockout KYSE-150 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population with targeted disruption of the human IL1R1 gene in the KYSE-150 esophageal squamous cell carcinoma line. This loss-of-function model enables study of interleukin-1 receptor type I (IL1R1) signaling without pharmacological interference or transient knockdown, providing a stable genetic background for functional analyses.
KYSE-150 is a widely used human epithelial cell line isolated from a poorly differentiated esophageal squamous cell carcinoma. It displays robust tumorigenic characteristics, including anchorage-independent growth and xenograft tumor formation, and its molecular landscape reflects key features of esophageal cancer, making it a relevant model for investigating oncogenic signaling and inflammatory crosstalk in this malignancy.
The IL1R1 gene product serves as the primary receptor for interleukin-1?? (IL1A) and interleukin-1?? (IL1B). Upon ligand engagement, IL1R1 heterodimerizes with the IL1RAP co-receptor, initiating recruitment of the MYD88 adaptor and activation of the kinases IRAK4 and IRAK1. These events promote TRAF6-dependent signaling that stimulates the NF-??B pathway and MAPK cascades, culminating in transcriptional upregulation of pro-inflammatory and oncogenic mediators such as IL6, TNF, CXCL8, MYC, and the NF-??B subunits NFKB1 and RELA. The natural antagonist IL1RN competitively inhibits this activation. In the polyclonal knockout cells, disruption of IL1R1 prevents receptor complex assembly and blocks the MYD88?CIRAK4?CIRAK1 axis, thereby extinguishing downstream NF-??B and MAPK-driven gene expression programs.
Esophageal squamous cell carcinoma progression is frequently associated with persistent inflammation and aberrant NF-??B activation. In KYSE-150 cells, IL1R1 signalling contributes to a pro-tumorigenic inflammatory milieu that enhances proliferation, migration, and invasiveness. By eliminating IL1R1 function, these polyclonal cells provide a clean experimental system to dissect interleukin-1-dependent oncogenic mechanisms and to assess how loss of IL-1 sensing impacts the malignant phenotype of esophageal carcinoma cells, independently of compensatory pathways that may confound ligand-blocking strategies.
These knockout cells are suitable for a range of assays, including Western blot analysis of phospho-p65 NF-??B, RT-qPCR quantification of IL6 and CXCL8 transcripts, and flow cytometric verification of surface IL1R1 loss. Migration and invasion assays, NF-??B luciferase reporter measurements, and cell viability or proliferation studies can directly link IL1R1 status to phenotypic outcomes. The model is also valuable for screening small-molecule inhibitors of the IL-1 pathway. For further information, please contact Ascent Research.
