The IL17RB Knockout 143B Polyclonal Cells constitute a loss-of-function model generated by CRISPR/Cas9-mediated gene disruption of the human IL17RB gene in the 143B osteosarcoma cell line. This product is supplied as a polyclonal knockout cell population, providing a heterogeneous pool of edited cells that allows researchers to interrogate the functional impact of IL17RB ablation while capturing biological variability. The CRISPR/Cas9 editing has been designed to disrupt the endogenous IL17RB locus, abolishing receptor expression and enabling detailed investigation of IL-25/IL-17B signaling in a bone cancer context.
The 143B cell line is a well-established human osteosarcoma model derived from a malignant bone tumor. These cells exhibit high tumorigenicity and are widely employed in studies of osteosarcoma biology, including tumor growth, invasion, metastasis, and therapeutic response. Their robust proliferation and invasive properties, coupled with a well-characterized genetic background, make 143B cells an ideal host for generating knockout models aimed at dissecting molecular mechanisms underlying bone cancer progression and drug resistance.
IL17RB encodes a transmembrane receptor that specifically binds the cytokines IL-17B and IL-25 (IL-17E). Upon ligand engagement, IL17RB forms a heterodimeric complex with IL17RA and recruits the adaptor protein Act1 (CIKS), which in turn engages TRAF6. This assembly triggers downstream activation of NF-??B, MAPK (ERK, JNK, and p38), and PI3K/AKT signaling cascades. Consequently, IL17RB signaling promotes the transcription of pro-inflammatory mediators such as IL-6, IL-8, CCL11 (eotaxin-1), and GM-CSF, thereby orchestrating type 2 immune responses and inflammation. The pathway is subject to regulation by upstream stimuli including TNF-?? and IL-1??, and is further modulated by interacting factors such as TRAF3.
In the context of 143B osteosarcoma, IL17RB may influence multiple malignant phenotypes, including proliferation, migration, invasion, and resistance to chemotherapy. Given the inherent aggressiveness of 143B cells and their ability to metastasize, particularly to bone, disrupting IL17RB provides a powerful tool to examine how IL-25/IL-17B-driven signals contribute to tumor progression and the bone marrow microenvironment. This knockout model enables the dissection of IL17RB-dependent crosstalk between inflammatory and oncogenic pathways, shedding light on potential therapeutic targets in osteosarcoma and other IL17RB-expressing cancers such as breast and lung carcinomas.
This IL17RB knockout polyclonal cell pool is suitable for a broad array of functional assays, including Western blotting, RT-qPCR, phospho-immunoblotting for ERK or NF-??B p65, and NF-??B luciferase reporter systems. ELISA-based detection of secreted IL-6 and IL-8 enables assessment of pro-inflammatory cytokine output, while Transwell assays evaluate migration and invasion. These cells also serve as a platform for drug sensitivity screens and bone metastasis modeling. For technical inquiries or custom requests, please contact Ascent Research.
