The IL27 Knockout UM-UC-3 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the UM-UC-3 human bladder urothelial carcinoma cell line. These cells feature targeted disruption of the IL27 gene, encoding the multifunctional cytokine interleukin-27. The polyclonal product format provides a heterogeneous pool of gene-edited cells, offering a stable loss-of-function model that circumvents single-cell clonal variation. This population is well suited for investigating IL27-mediated signaling and its role in tumor biology.
UM-UC-3 is a well-characterized model of invasive bladder cancer, originally derived from a male patient with high-grade transitional cell carcinoma. The cell line retains key characteristics of urothelial carcinoma, including epithelial morphology and tumorigenicity, making it a relevant system for studying bladder cancer pathogenesis and therapeutic responses. Its genetic background encompasses mutations common in bladder malignancies, supporting its utility in oncogenic research.
IL27 is a heterodimeric cytokine (EBI3 and p28) that signals via IL-27R?? (WSX-1) and gp130, activating JAK1/2 and phosphorylating STAT1/3. These transcription factors regulate targets including T-bet, IL-10, and PD-L1. IL27 exerts dual functions: it promotes Th1 differentiation through STAT1-mediated T-bet expression, while suppressing Th2 and Th17 responses and inhibiting regulatory T cell development via STAT3. Upstream, its expression is induced by IFN-gamma, TLR ligands, CD40 ligand, and microbial products. Negative regulators SOCS1 and SOCS3 modulate signaling intensity. This network places IL27 at a central node of pro- and anti-inflammatory pathways, with direct consequences for tumor immune surveillance.
In the UM-UC-3 bladder cancer setting, endogenous IL27 production can shape the tumor microenvironment by affecting cytokine secretion, immune recruitment, and checkpoint molecule expression. Disrupting IL27 in this polyclonal knockout model enables dissection of autocrine and paracrine effects of tumor-derived IL27. Given that IL27 regulates PD-L1, the cells are particularly valuable for immune evasion studies. Moreover, the knockout’s origin in a high-grade carcinoma provides insights into how IL27 signaling contributes to invasive bladder cancer aggressiveness, with the polyclonal nature reducing clonal artifacts.
These polyclonal knockout cells support diverse experimental approaches, including western blotting for STAT1/STAT3 phosphorylation, RT-qPCR for T-bet, IL-10, and PD-L1 transcripts, and ELISA for secreted cytokines. Co-culture with immune cells paired with flow cytometry allows profiling of IL27-dependent T-cell differentiation. MTT assays assess cell viability changes upon IL27 disruption, especially with chemotherapeutics. Applications extend to immune checkpoint studies and JAK-STAT inhibitor screening. For product details or custom inquiries, contact Ascent Research.
