IL17RB knockout KYSE-150 polyclonal cells are a CRISPR/Cas9-edited polyclonal population derived from the human esophageal squamous cell carcinoma cell line KYSE-150, with targeted disruption of the IL17RB gene. This heterogeneous pool of gene-edited cells provides a loss-of-function model for studying IL17RB inactivation. CRISPR/Cas9-mediated disruption eliminates functional IL-17RB receptor, thereby abrogating signaling by the ligands IL-17B and IL-25.
The KYSE-150 cell line originates from a poorly differentiated human esophageal squamous cell carcinoma and serves as a well-established model for ESCC research. These cells display characteristic features including aberrant proliferation, migration, and dysregulated inflammatory signaling, retaining the genomic and phenotypic properties of the original tumor.
IL17RB encodes the interleukin-17 receptor B, which pairs with IL-17RA to bind the ligands IL-17B and IL-25. Ligand engagement triggers recruitment of the adaptor Act1 (TRAF3IP2) and the ubiquitin ligase TRAF6, leading to activation of the TAK1-IKK cascade and subsequent NF-??B signaling, as well as parallel MAPK pathways involving p38, JNK, and ERK. These pathways drive transcription of pro-inflammatory mediators including IL-8, CXCL1, and CCL20. Additional regulators such as TNF-?? and IL-1?? modulate IL17RB expression and can synergize with receptor activation. The adaptor IRAK1 also intersects with this signaling complex.
In KYSE-150 cells, IL17RB-mediated signaling promotes a tumor-supportive microenvironment through induction of cytokines and chemokines. Knockout of IL17RB abrogates NF-??B and MAPK pathway activation, reducing expression of key inflammatory factors and impairing processes such as cell proliferation, migration, and immune evasion. The polyclonal knockout pool captures a broad spectrum of gene-editing events, minimizing clonal bias while reliably conferring loss of receptor function.
This model supports diverse experimental workflows: western blotting and flow cytometry for receptor expression verification, RT-qPCR and Sanger sequencing for transcript and indel analysis, NF-??B reporter and phospho-signaling assays for pathway assessment, and cytokine/chemokine ELISA for secreted factor profiling. Functional assays including proliferation, migration, and invasion can elucidate IL17RB roles in tumor biology. Transcriptomic analyses via RNA-seq enable global expression profiling. Applications include investigating IL-17B/IL-25 signaling in ESCC inflammation, evaluating IL17RB as a therapeutic target, and screening for receptor inhibitors. For further information, please contact Ascent Research.
