The IL1R1 Knockout UM-UC-3 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human bladder carcinoma cell line UM-UC-3, targeting the IL1R1 gene. This polyclonal product provides a heterogeneous knockout model in which IL1R1 gene disruption is achieved through CRISPR/Cas9-mediated gene editing, enabling loss-of-function studies without the clonal artifacts often associated with single-cell-derived knockouts. The cell population is designed for researchers investigating IL-1 receptor biology and its contributions to disease mechanisms in a bladder cancer context.
The host cell line, UM-UC-3, originated from a male patient diagnosed with urinary bladder transitional cell carcinoma and exhibits characteristic epithelial morphology. As a widely employed model for bladder cancer research, UM-UC-3 cells retain key features of the primary tumor, including invasive potential and responsiveness to inflammatory stimuli, making them a relevant platform for exploring tumor cell signaling, drug sensitivity, and the interplay between inflammation and malignancy.
IL1R1 encodes the type I interleukin-1 receptor, which serves as the primary signaling receptor for the pro-inflammatory cytokines IL-1?? and IL-1??. Upon ligand binding, IL1R1 heterodimerizes with the co-receptor IL1RAP, recruiting the adaptor proteins MYD88, IRAK4, and IRAK1. This assembly activates the E3 ubiquitin ligase TRAF6, leading to downstream activation of the TAK1 kinase complex. TAK1 subsequently phosphorylates the IKK complex, triggering NF-??B nuclear translocation, and also stimulates MAPK cascades (JNK/p38), culminating in AP-1 activation. The resulting transcriptional program upregulates numerous inflammatory and matrix-modifying factors, including IL-6, IL-8, TNF, COX-2, and MMPs.
In the context of UM-UC-3 bladder carcinoma cells, IL1R1-mediated signaling is implicated in promoting inflammation-driven tumor progression, proliferation, and resistance to therapy. Disruption of IL1R1 in this polyclonal knockout population ablates the ability to respond to IL-1??/??, thereby blocking recruitment of IL1RAP and downstream adaptors, inhibiting NF-??B and MAPK pathway activation, and attenuating the expression of pro-inflammatory mediators. This model enables researchers to unambiguously assign IL-1-specific effects within the complex signaling networks of bladder cancer cells.
This knockout product is suited for a broad range of functional and mechanistic studies. Typical applications include examining IL-1-dependent tumor cell proliferation, migration, and invasion using real-time cell analysis or transwell assays; assessing signal transduction by western blotting for phospho-NF-??B, phospho-JNK, or total protein levels of target gene products; quantifying transcriptional responses via RT-qPCR for IL-6, IL-8, or TNF; and measuring secreted cytokines by ELISA following IL-1?? stimulation. Additionally, the cells can be employed in NF-??B luciferase reporter assays, drug sensitivity screens, and co-culture experiments to evaluate the contribution of IL1R1 to stromal?Ctumor interactions. For further technical information, please contact Ascent Research.
