IL17RB Knockout NCI-H1703 Polyclonal Cells constitute a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the NCI-H1703 human lung squamous cell carcinoma line. This knockout model provides a heterogeneous pool of cells with targeted disruption of the IL17RB locus, enabling population-based loss-of-function analyses. The polyclonal format is suitable for experiments that do not require clonal homogeneity, such as bulk signaling studies, cytokine profiling, and drug response assays. By ablating IL17RB expression across a mixed cellular background, researchers can interrogate the functional consequences of receptor loss in a context that reflects the inherent diversity of cultured cancer cells.
NCI-H1703 is a well-characterized non-small cell lung cancer (NSCLC) cell line originally derived from a patient with squamous cell carcinoma of the lung. This line retains key molecular and phenotypic features of the primary tumor, including alterations in tumor suppressor pathways and proliferative signaling networks. As an adherent, epithelial-like cell line, NCI-H1703 is commonly employed in lung cancer research to study mechanisms of oncogenesis, metastasis, and therapeutic resistance. Its origin from a smoking-associated cancer type makes it particularly relevant for investigations into inflammation-driven lung carcinogenesis and the tumor-immune microenvironment.
IL17RB encodes the receptor for the cytokines IL-17B and IL-25 (also known as IL-17E), which play critical roles in allergic inflammation and host defense. Upon ligand binding, IL17RB recruits the adaptor protein Act1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6, initiating signaling cascades that culminate in the activation of NF-??B and mitogen-activated protein kinases (MAPKs). Key downstream transcription factors include NFKB1/RELA and phosphorylated MAPK1 (ERK2) and MAPK3 (ERK1), which drive the expression of pro-inflammatory genes. IL17RB signaling also stimulates STAT3 phosphorylation, linking it to broader cytokine networks. Target genes induced by this pathway include IL-8 (CXCL8), IL-6, and the chemokine CCL20, which promote neutrophil and dendritic cell recruitment.
In the context of NCI-H1703 lung carcinoma cells, the IL17RB pathway may contribute to tumor-associated inflammation and modulation of the tumor microenvironment. Ligand stimulation with IL-25 has been shown to activate NF-??B and ERK in lung epithelial cells, potentially promoting survival, cytokine secretion, and chemoresistance. Disruption of IL17RB in this squamous cell carcinoma model allows precise dissection of the IL-25/IL-17RB axis and its impact on NSCLC cell behavior, including proliferation, migration, and interaction with immune cells. This knockout system thus provides a relevant platform to investigate how IL17RB-mediated signaling influences lung cancer pathophysiology and inflammatory comorbidities such as chronic rhinosinusitis.
These polyclonal knockout cells are well-suited for a range of downstream applications. Confirmation of IL17RB knockout can be achieved via RT-qPCR and western blotting for IL17RB protein. Functional studies may involve stimulation with recombinant IL-25 followed by phospho-NF-??B or phospho-ERK western blots, as well as ELISA quantification of secreted IL-6 and IL-8. Cell migration assays and drug sensitivity testing can elucidate the receptor’s role in motile and chemoresistant phenotypes. Additionally, the cells can be integrated into functional genomic screens or used in co-culture models to explore the crosstalk between lung cancer cells and immune components, particularly in allergic inflammation and asthma research. For inquiries, please contact Ascent Research.
