The IL27 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population in the AGS human gastric adenocarcinoma cell line, designed for loss-of-function studies of the IL27 gene. This gene-edited model disrupts IL-27 expression, enabling researchers to investigate the cytokine??s role in gastric epithelial cell biology, immune modulation, and tumor progression. As a polyclonal population, it reflects the heterogeneous editing outcomes of CRISPR/Cas9, providing a robust system for functional studies without clonal selection artifacts. The knockout cells are well-suited for high-content assays including signaling pathway analysis, cytokine profiling, and drug discovery screens.
The AGS cell line, isolated from a patient with gastric cancer, is a widely characterized model for studying gastric adenocarcinoma, mucosal biology, and pharmacological responses. Its epithelial origin and consistent growth in culture make it an ideal host for cytokine signaling investigations. AGS cells endogenously express receptors for cytokines such as IL-27, facilitating the study of autocrine and paracrine signaling networks. Use of this cell background allows researchers to explore IL-27??s contributions to gastric cancer pathophysiology within a relevant human cell context.
IL-27 is a heterodimeric cytokine consisting of the IL27A (p28) and EBI3 subunits, which signals through a receptor complex of IL27RA (WSX-1) and IL6ST (gp130). Ligand binding triggers activation of JAK1 and JAK2, leading to phosphorylation of STAT1 and STAT3 transcription factors. Downstream, STAT1/STAT3 induce expression of T-bet and IL-12R??2, promoting Th1-type immune responses, while simultaneously suppressing ROR??t and IL-17 production to inhibit Th17 differentiation. Additionally, IL-27 stimulates IL-10 expression and is regulated by upstream signals such as TLR ligands, IFN-??, NF-??B, IRF1, and IRF3.
In the gastric cancer microenvironment, IL-27 can exert pleiotropic effects on both tumor and immune cells. In AGS cells, disruption of endogenous IL27 may alter STAT1 and STAT3 activation profiles, impacting cell proliferation, apoptosis, and cytokine secretion. This knockout model enables dissection of IL-27??s cell-autonomous roles in gastric epithelial cells, distinct from its immunomodulatory functions. By comparing wild-type and knockout populations, researchers can evaluate contributions to tumor growth, invasion, and response to therapeutics, offering insights into IL-27 as a potential target in gastric cancer.
This polyclonal knockout product is applicable for diverse experimental strategies including western blotting and RT-qPCR to confirm IL27 disruption, ELISA and phospho-STAT1/STAT3 flow cytometry to assess signaling outputs, and functional assays for proliferation, apoptosis, and co-culture with immune cells. Gene expression profiling via RNA-seq can reveal broader pathway alterations. These cells support screening for IL-27 pathway modulators and investigating mechanisms of immune evasion. For additional information or custom requirements, please contact Ascent Research.
