The IL1R1 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human TE1 esophageal squamous cell carcinoma cell line. The knockout pool comprises a heterogeneous mix of cells with disrupted IL1R1 alleles, generated through CRISPR/Cas9-mediated gene editing. This polyclonal product is designed for functional genomics and signaling research, providing a robust loss-of-function model without the need for single-cell cloning.
TE1 is a poorly differentiated human esophageal squamous cell carcinoma cell line, widely used as a model for esophageal epithelial carcinoma. These cells exhibit characteristic features of aggressive esophageal cancer, including rapid proliferation and invasive potential. The TE1 line serves as an ideal platform for investigating the molecular mechanisms driving esophageal carcinogenesis and for evaluating therapeutic interventions.
IL1R1 encodes the type I interleukin-1 receptor, a critical initiator of pro-inflammatory signaling. Upon binding of its ligands IL1A or IL1B, IL1R1 recruits the co-receptor IL1RAP, facilitating the assembly of a signaling complex that includes the adaptor MYD88 and kinases IRAK4 and IRAK1. This complex triggers the activation of TRAF6, which in turn leads to the phosphorylation and degradation of NFKBIA, releasing NF-kB dimers such as RELA. Concurrently, the MAPK cascade, including MAPK3/1, is stimulated, resulting in the activation of transcription factors JUN and FOS. These pathways converge to drive transcription of downstream targets like IL6, CXCL8, and matrix metalloproteinases (MMPs), mediating inflammatory and immune responses. Negative regulation is provided by IL1RN, an endogenous antagonist.
In the context of TE1 esophageal cancer cells, IL-1 signaling has been implicated in tumor-promoting inflammation, cell migration, and resistance to apoptosis. Disruption of IL1R1 in this background abrogates the cellular responses to IL-1?? and IL-1??, enabling researchers to dissect the contribution of IL-1 signaling to esophageal cancer progression. This knockout model is particularly valuable for studying how the inflammatory microenvironment influences malignant phenotypes, including invasion and immune evasion, and for validating IL1R1 as a potential therapeutic target.
Representative applications include Western blotting for NF-kB pathway activation (e.g., RELA phosphorylation), RT-qPCR quantification of IL6 and CXCL8 expression, and ELISA measurement of secreted cytokines. Phospho-signaling analysis can be performed to assess MAPK pathway activity, while flow cytometry verifies loss of surface IL1R1. Functional assays such as migration and invasion studies can directly test the impact of IL1R1 knockout on metastatic behavior. Additionally, these cells are suitable for co-immunoprecipitation to examine the interaction between IL1R1 and IL1RAP, and for drug sensitivity profiling with IL-1 inhibitors (e.g., anakinra). For further details, please contact Ascent Research.
