The IL27 Knockout KYSE-30 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the well-differentiated KYSE-30 human esophageal squamous cell carcinoma line. This product is designed to disrupt the endogenous IL27 gene, creating a loss-of-function model for studying IL27-mediated signaling in esophageal cancer biology. The polyclonal nature ensures a heterogeneous knockout pool, suitable for experiments where population-level effects of IL27 disruption are investigated. Researchers can employ this model to dissect the role of IL27 in tumor immunity and cytokine signaling without the constraints of single-cell clones.
The KYSE-30 cell line was established from a well-differentiated esophageal squamous cell carcinoma resected from a 64-year-old Japanese male. It serves as a classic model for esophageal squamous cell carcinoma research, retaining key molecular features of the primary tumor. KYSE-30 cells are widely used to study oncogenic pathways, drug responses, and tumor?Cimmune interactions in the context of esophageal cancer. Their robust growth characteristics and well-characterized genetic background make them an ideal host for gene-knockout studies.
IL27 is an immunomodulatory cytokine composed of EBI3 and IL27p28 subunits, which signals through the heterodimeric receptor IL27RA (WSX-1)/gp130. Ligand binding activates JAK1 and JAK2, leading to phosphorylation of STAT1 and STAT3. These transcription factors regulate targets such as T-bet, SOCS1, SOCS3, and IL-12R??2, promoting Th1 differentiation and suppressing Th17/Treg development. IL27 expression is induced by LPS, TLR4 agonists, IFN-??, and NF-??B via IRF1, placing it at the convergence of innate immune activation and adaptive T-cell responses.
In KYSE-30 cells, IL27 signaling may influence tumor-intrinsic JAK-STAT activation and cytokine secretion shaping the microenvironment. IL27 knockout abolishes STAT1/STAT3 phosphorylation, impairing downstream programs that could affect proliferation, survival, or immune evasion. This model enables dissection of whether IL27 from esophageal carcinoma cells contributes to immune surveillance or tumor progression, and it facilitates co-culture studies with immune cells to examine functional crosstalk.
Typical applications include esophageal cancer immunology studies comparing IL27 knockout and wild-type cells in PBMC co-cultures to assess T-cell polarization or cytokine secretion. The model is suited for drug screening targeting TLR4 or JAK-STAT effectors. Researchers can perform Western blotting for phospho-STAT1/STAT3, RT-qPCR for IL27 and targets, ELISA for cytokine secretion, flow cytometry for surface markers, migration assays, and RNA-seq for transcriptomic profiling. This polyclonal knockout population provides a versatile tool for investigating tumor-intrinsic immune regulation and preclinical evaluation of pathway modulators. For additional details or technical support, please contact Ascent Research.
