The IL27 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout population with disruption of the IL27 gene in HGC-27 human gastric carcinoma cells. This loss-of-function model enables investigation of interleukin-27 (IL27) in gastric epithelial biology, immune regulation, and cancer signaling. The polyclonal format provides a heterogeneous pool of edited alleles, avoiding clonal bias while maintaining relevant genetic diversity.
HGC-27 is a poorly differentiated human gastric adenocarcinoma cell line of lymph node metastasis origin, widely used as a model for gastric epithelial function and cancer biology. These adherent epithelial cells retain key signaling networks controlling proliferation, migration, and apoptosis. As a gastric cancer cell line, HGC-27 produces and responds to cytokines, making it a physiologically relevant host for IL27 knockout studies, particularly for investigating mechanisms of invasion and immune evasion within the tumor microenvironment.
IL27 is a heterodimeric cytokine composed of EBI3 and IL27A subunits, signaling via the IL27RA/gp130 receptor complex and the kinases JAK1 and TYK2 to phosphorylate STAT1 and STAT3. Its expression is induced by stimuli such as LPS, CpG DNA, CD40L, IFN-??, and IL-1?? through NF-??B, IRF1, and IRF3. Downstream, IL27 promotes TBX21 expression for Th1 responses and induces IL10 while inhibiting Th17 differentiation. In tumor cells, it regulates CD274 (PD-L1), CXCL10, BCL2 family members, and MMPs. Negative regulators include SOCS1 and SOCS3. CRISPR-mediated disruption of IL27 in HGC-27 cells abrogates this signaling axis, enabling dissection of IL27-dependent molecular events.
In HGC-27 cells, IL27 exerts pleiotropic effects balancing pro- and anti-tumorigenic outcomes via STAT1/STAT3 activation. Knockout of IL27 is anticipated to alter phosphorylation of these STATs, impacting transcription of genes involved in proliferation, apoptosis, and migration. Additionally, disrupted IL27 function may modify PD-L1 surface levels and cytokine/chemokine secretion, thereby reshaping autocrine and paracrine signaling in the tumor microenvironment. This model is thus valuable for studying how IL27 contributes to gastric cancer progression and immune modulation.
The knockout cells are suitable for a range of assays including Western blot and RT-qPCR for IL27 expression, phospho-STAT1/3 analysis, apoptosis and proliferation assays (Annexin V, MTT), transwell migration, and ELISA or flow cytometry for targets such as IL10, CXCL10, and PD-L1. They can be employed in STAT reporter assays, RNA-seq transcriptomics, drug sensitivity testing, and tumor-immune interaction models. These applications support investigations into gastric cancer biology, cytokine signaling, and therapeutic targeting. For technical assistance, contact Ascent Research.
