The IL17RB Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the IL17RB gene in a non-small cell lung carcinoma (NSCLC) background. This loss-of-function model allows detailed study of IL17B/IL25 receptor signaling without endogenous IL17RB expression. As a polyclonal pool, the product represents a heterogeneous collection of edited alleles, avoiding clonal bias and reflecting the diverse editing outcomes typical of CRISPR-mediated gene disruption in bulk cells.
The parental NCI-H1299 cell line is a well-characterized epithelial lung carcinoma line derived from metastatic NSCLC. It is widely used as a model for lung adenocarcinoma, exhibiting key oncogenic features and responsiveness to cytokine stimulation. Its established transcriptomic and signaling context provides a reproducible platform for interrogating gene function in cancer-related inflammation and tumor biology.
IL17RB encodes the receptor for IL17B and IL25. Ligand binding triggers heterodimerization with IL17RA, recruitment of ACT1 (TRAF3IP2), and activation of TRAF6-TAK1, leading to NF-??B and MAP kinase (ERK, JNK, p38) cascades. Downstream targets include pro-inflammatory and Th2 cytokines: IL6, IL8, CXCL1, IL4, IL5, IL13. TNF-?? and IL-1?? upregulate receptor signaling. In knockout cells, loss of IL17RB prevents ACT1 recruitment, abolishing ligand-induced NF-??B/MAPK activation and cytokine production.
In NCI-H1299 NSCLC cells, IL17RB may contribute to tumor-promoting inflammation and a Th2-skewed microenvironment that facilitates immune evasion and tumor progression. Knockout enables dissection of IL17B/IL25-specific effects on cytokine secretion, cell migration, and survival, and reveals potential compensatory mechanisms. This model is particularly useful for studying IL17RB-dependent pathways in lung cancer and their interaction with tumor-stromal signals.
Typical applications include western blot analysis of signaling effectors (phospho-NF-??B, phospho-ERK), RT-qPCR quantification of target genes (IL6, IL8, IL4), ELISA-based measurement of secreted cytokines, and NF-??B luciferase reporter assays following IL17B/IL25 stimulation. Co-immunoprecipitation confirms disrupted receptor?Cadaptor interactions. Functional assays such as wound-healing migration and apoptosis complement transcriptome profiling by RNA-seq, supporting drug screening and mechanistic studies. For further information, please contact Ascent Research.
