The IL11 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the TE1 human esophageal squamous cell carcinoma line, designed for loss-of-function analysis of interleukin-11 (IL-11). This heterogeneous pool of cells harbors targeted disruptions in the IL11 gene introduced by CRISPR/Cas9-mediated gene editing, offering a robust model to study IL-11 signaling without the clonal selection biases of monoclonal lines.
The parental TE1 cell line is a well-characterized human esophageal squamous cell carcinoma model established from a primary esophageal tumor. TE1 cells exhibit typical squamous carcinoma features, including epithelial morphology and activated oncogenic pathways, and are widely used in esophageal cancer research. This host context provides a clinically relevant platform for exploring cytokine-mediated tumor progression mechanisms.
IL-11 is a pleiotropic member of the IL-6 cytokine family that signals via a heterodimeric receptor composed of IL-11RA and GP130 (IL6ST). Ligand binding triggers activation of JAK1 and JAK2, leading to phosphorylation of STAT3 and STAT1. Activated STAT3 translocates to the nucleus and transcriptionally upregulates key targets such as Cyclin D1, BCL2, SOCS3, and VEGF, promoting cell cycle progression, survival, and angiogenesis. Concurrently, JAK-dependent signaling activates the MAPK/ERK pathway, resulting in ERK1/2 phosphorylation and mitogenic gene expression. IL-11 expression is controlled by upstream regulators including TGF-??, IL-1, TNF, HIF1A, NF-??B, and AP-1, linking inflammatory and hypoxic cues. IL-11 also promotes epithelial-mesenchymal transition and is implicated in fibrosis and cancer progression.
In esophageal squamous cell carcinoma, IL-11-driven activation of STAT3 and ERK1/2 enhances tumor cell proliferation, migration, invasion, and resistance to apoptosis. The TE1 knockout model provides a genetically defined system to dissect these processes by ablating IL-11-mediated autocrine and paracrine signaling. Elimination of IL-11 disrupts downstream STAT3 and ERK activity, diminishing expression of pro-survival and pro-angiogenic factors. This facilitates investigation of IL-11-dependent crosstalk with the tumor microenvironment and exploration of combination therapies targeting the JAK/STAT or MEK/ERK axes. The polyclonal population maintains editing heterogeneity, reflecting a more representative knockout landscape than clonal isolates.
This product is ideally suited for comprehensive functional genomics studies in esophageal cancer. Researchers can employ RNA-seq transcriptomic profiling to map IL-11-regulated gene networks, complemented by targeted validation via phospho-STAT3 western blotting and RT-qPCR analysis of known STAT3 targets. Phenotypic assays for cell proliferation, migration, and invasion directly measure the impact of IL-11 loss on tumor-cell behavior. The polyclonal knockout population also enables pooled CRISPR screening approaches and studies of intratumoral heterogeneity. For further details and support, please contact Ascent Research.
