The IL17RB Knockout AGS Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma epithelial cell line, providing a loss-of-function model for the interleukin 17 receptor B (IL17RB) gene. This pooled knockout cell population, generated by CRISPR/Cas9-mediated gene disruption, enables functional interrogation of IL17RB-dependent signaling in a gastric epithelial context without the confounding effects of clonal selection or specific editing patterns. The polyclonal format captures a spectrum of editing events across the cell population, recapitulating heterogeneous knockout efficiencies ideal for bulk assays and pathway-level analyses.
The parental AGS cell line is a widely employed model of gastric adenocarcinoma, originally established from a primary tumor of a female patient. These epithelial cells exhibit hallmark features of gastric cancer, including aberrant proliferative and migratory capacities, and retain key signaling circuitry relevant to gastric tumor biology. The AGS background provides a physiologically appropriate host for studying IL17RB function in gastric cancer, as this receptor is implicated in tumor cell proliferation, survival, and inflammatory microenvironment modulation within the gastric epithelium.
IL17RB encodes a single-pass transmembrane receptor that is activated by the cytokines IL-17B and IL-25 (IL-17E), triggering pro-inflammatory and type 2 immune responses. Upon ligand binding, IL17RB heterodimerizes with IL17RA and recruits the adaptor protein Act1 (TRAF3IP2), which in turn engages TRAF6 to propagate downstream signaling. This axis activates the NF-??B pathway through the IKK complex and stimulates MAPK cascades, including ERK1/2 and JNK (MAPK8), leading to the transcriptional induction of inflammatory mediators such as IL-8, IL-6, CXCL1, and the anti-apoptotic factor BIRC5. Upstream regulators of this pathway include TNF-??, which can synergize with IL-17 signals, further potentiating the inflammatory output.
In AGS gastric adenocarcinoma cells, IL17RB-mediated signaling represents a critical node linking inflammatory cues to epithelial cell responses associated with tumor progression. The knockout of IL17RB in this cell line allows researchers to dissect the receptor’s contribution to NF-??B and MAPK/ERK pathway activation, cytokine production, and downstream phenotypes such as proliferation, migration, and invasion. Given the established roles of IL-17 family cytokines in gastric inflammation and carcinogenesis, this model is particularly relevant for investigating how IL17RB influences gastric cancer cell behavior and responsiveness to niche-derived signals.
This IL17RB knockout product is suited for a broad range of experimental applications. It can be employed in functional assays including RT-qPCR and Western blotting to validate target gene disruption and assess downstream effector expression, phospho-NF-??B ELISA to quantify pathway activity, and immunofluorescence or flow cytometry to examine receptor surface expression. For phenotypic readouts, the knockout cells enable MTT proliferation assays, wound healing and transwell invasion assays to evaluate metastatic potential, and apoptosis assays in the context of pathway inhibition. Additionally, the polyclonal population can serve as a screening tool for small-molecule inhibitors targeting IL-17 signaling or as a negative control in RNA-seq studies comparing wild-type and knockout transcriptomes. For additional technical details or inquiry, please contact Ascent Research.
