The IL17RB Knockout CAL-27 Polyclonal Cells product is a targeted loss-of-function model generated through CRISPR/Cas9-mediated disruption of the interleukin-17 receptor B (IL17RB) gene in the CAL-27 human tongue squamous cell carcinoma cell line. This engineered population consists of polyclonal knockout cells in which the IL17RB locus has been disrupted, providing a genetically stable and renewable resource for dissecting IL17RB-dependent signaling mechanisms. The polyclonal nature of the knockout ensures representation of diverse editing outcomes while maintaining overall functional nullity of the target gene, suitable for reproducible downstream applications in cancer and inflammation research.
CAL-27 is an adherent epithelial cell line originally established from a squamous cell carcinoma of the tongue in a 56-year-old Caucasian male. Widely employed as a model system for oral cancer, CAL-27 cells retain key characteristics of tongue squamous cell carcinoma, including robust proliferation, invasive potential, and responsiveness to inflammatory cues. This host cell background offers a clinically relevant context to evaluate the contributions of IL17RB to malignant phenotypes and tumor?Cimmune interactions in the oral cavity.
IL17RB encodes the receptor for the cytokines IL-17B and IL-25 (also known as IL-17E). Upon ligand binding, IL17RB heterodimerizes with IL-17RA and recruits the adaptor proteins TRAF3IP2 (ACT1) and TRAF6, which subsequently trigger downstream activation of the NF-??B and MAPK signaling cascades. Representative pathway components include IKBKB and RELA in the NF-??B branch, and MAPK1 (ERK2) and MAPK3 (ERK1) in the MAPK branch, leading to transcriptional induction of pro-inflammatory effectors such as JUN, IL6, and CXCL8. This signaling axis is integral to type 2 immune responses and tissue inflammation, and its dysregulation has been implicated in allergic diseases and multiple carcinomas.
In the CAL-27 oral cancer model, IL17RB-mediated signaling is thought to promote tumor-associated inflammation and support malignant progression by driving cytokine and chemokine expression. Disrupting IL17RB in these cells allows researchers to interrogate the receptor’s role in modulating NF-??B and MAPK pathway activity, as well as downstream phenotypic outcomes including proliferation, migration, and invasion. The knockout model thus serves as a powerful tool to elucidate how IL?25/IL?17RB paracrine or autocrine loops contribute to the aggressive behavior of tongue squamous cell carcinoma and to identify potential therapeutic vulnerabilities.
This CRISPR/Cas9-edited polyclonal knockout cell product is designed for a range of experimental applications in cancer biology, inflammation research, and drug target validation. Common downstream assays include Western blotting and RT-qPCR for pathway component expression, NF-??B luciferase reporter assays to quantify transcriptional activity, cytokine ELISA (e.g., IL-6, CXCL8) for secretory profiles, proliferation and migration/invasion assays for functional phenotyping, and immunofluorescence for subcellular localization studies. The IL17RB Knockout CAL-27 Polyclonal Cells empower detailed mechanistic studies of IL?25/IL?17RB signaling and its interplay with oral cancer pathology. For additional technical specifications or custom engineering inquiries, please contact Ascent Research.
