The IL27 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human esophageal squamous cell carcinoma line KYSE-150, featuring targeted disruption of the IL27 gene. The polyclonal format provides a heterogeneous pool of gene-edited cells without clonal selection, suitable for studying IL27-mediated signaling in a cancer cell context and avoiding artifacts of single-cell cloning.
The parental KYSE-150 line is a poorly differentiated human esophageal squamous cell carcinoma model established from a Japanese patient. KYSE-150 cells are widely used for ESCC pathogenesis research, exhibiting epithelial morphology and typical malignant features, including dysregulated growth, migration, and invasion. Their esophageal squamous origin provides a human-relevant platform for studying oncogenic signaling and tumor microenvironment interactions.
IL27 encodes the p28 subunit of the heterodimeric cytokine IL-27, which partners with EBI3. IL-27 signals through a receptor complex of IL27RA and gp130, activating JAK1, JAK2, and TYK2, and subsequently phosphorylating STAT1 and STAT3. Downstream, it induces T-bet, IL-10, and SOCS3, while suppressing RORC to inhibit Th17 differentiation. Upstream, IL27 expression is regulated by TLR4 ligands, IFN-??, NF-??B, and IRF1. This cytokine modulates adaptive immunity by promoting Th1 and Treg responses and can exert pleiotropic effects on cancer cells via STAT-dependent transcriptional programs.
In KYSE-150 cells, endogenous IL27 may drive autocrine/paracrine signaling affecting tumor cell proliferation, migration, and immune crosstalk. IL27 disruption creates a loss-of-function model for dissecting its role in ESCC cell behavior and STAT1/STAT3-dependent gene networks, including SOCS3 feedback. This model is instrumental for investigating IL27??s contribution to immune evasion and inflammation-regulated cancer progression within the esophageal tumor microenvironment.
Research applications include western blotting and RT-qPCR for knockout validation, RNA-seq for transcriptome analysis, and phospho-STAT assays to probe signaling changes. Functional assays??proliferation, migration, invasion??quantify aggressiveness. Co-cultures with immune cells and cytokine ELISA/flow cytometry evaluate tumor-immune interactions, while the model aids drug resistance studies and compound screening targeting IL27 pathways. For more information, contact Ascent Research.
