The IL17RB Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HCT 116, providing a loss-of-function model for IL17RB. This polyclonal pool is generated via CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous population with targeted IL17RB knockout. It offers a genetically defined system to study IL17RB signaling in a cancer-relevant context without clonal selection constraints.
HCT 116 is a human colorectal adenocarcinoma epithelial cell line harboring a KRAS mutation that drives constitutive MAPK pathway activity. This fast-growing, adherent model retains key colorectal cancer features, including aberrant proliferation, apoptosis resistance, and tumorigenic potential. The KRAS mutation makes it valuable for studying oncogenic and inflammatory pathway crosstalk. IL17RB knockout in this background enables precise investigation of IL-25-driven signaling interplay with intrinsic oncogenic signals.
IL17RB encodes the receptor for IL-25 (IL-17E), a type 2 inflammatory cytokine. IL-25 binding induces heterodimerization with IL-17RA, recruitment of adaptor TRAF3IP2 (Act1) and ubiquitin ligase TRAF6, activating NF-??B and MAPK cascades. This leads to phosphorylation of NFKB1, MAPK3 (ERK1), and MAPK1 (ERK2), and transcriptional induction of IL-6, IL-8, CXCL1, and G-CSF. These mediators drive immune cell recruitment, tissue remodeling, and tumor-promoting inflammation. IL17RB disruption abolishes IL-25 signal transduction, impairing downstream network activation.
In HCT 116, IL17RB expression is linked to tumor-promoting inflammation and metastasis. The KRAS mutation amplifies MAPK signaling, potentially synergizing with IL-25/IL17RB-mediated NF-??B activation to enhance cytokine secretion, migration, and survival. Eliminating IL17RB uncouples IL-25-driven inflammation from oncogenic signals, enabling evaluation of type 2 inflammatory contributions to colorectal cancer progression and therapeutic targeting of the IL-25/IL17RB axis.
The cells are ideal for cancer progression models, inflammatory disease research, IL-25 signaling dissection, and drug target validation. Representative assays include western blotting for protein and phospho-protein detection, RT-qPCR for transcriptional profiling, phospho-flow cytometry for signaling analysis, migration assays, and ELISA for IL-6 and IL-8 secretion. The polyclonal nature captures a broad range of knockout effects, facilitating functional screens and population-based studies. For further information, contact Ascent Research.
