The IL17RB Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population that disrupts IL17RB gene expression in the A2780 human ovarian cancer cell line. This mixed pool of edited cells provides a robust loss-of-function model for studying IL17RB signaling. The polyclonal format minimizes biases from clonal variation and ensures broad genetic ablation within the population, making it ideal for population-level functional studies in ovarian cancer research.
A2780 is a well-characterized epithelial ovarian cancer cell line originally derived from an untreated patient with endometrioid adenocarcinoma. It serves as a widely used model for investigating ovarian cancer pathogenesis, drug sensitivity, and metastatic mechanisms. Disrupting IL17RB in this context allows precise dissection of its contributions to ovarian cancer cell-autonomous functions, including proliferation, survival, and resistance to chemotherapy.
IL17RB encodes a receptor for IL-25 and IL-17B, which recruits ACT1 and TRAF6 upon ligand binding, leading to activation of NF-??B via the TAK1-IKK complex and MAPK pathways (JNK, p38, ERK). This signaling drives expression of Th2 cytokines (IL-4, IL-5, IL-13), chemokines (CXCL1, CCL20), and G-CSF. These mediators promote Th2-type inflammation and create an immunosuppressive tumor microenvironment, facilitating cancer progression.
In A2780 cells, aberrant IL17RB signaling likely enhances ovarian cancer aggressiveness by promoting proliferation, metastasis, and drug resistance through the IL-25/IL17RB/ACT1/TRAF6 axis. The polyclonal knockout cells enable rigorous examination of how loss of IL17RB alters NF-??B and MAPK pathway activity, downstream cytokine profiles, and cellular migration. They are particularly valuable for studying the tumor microenvironment, as IL17RB-driven cytokine networks can modulate immune cell recruitment and inflammation within ovarian tumors.
Applications include Western blotting for phospho-NF-??B and phospho-MAPK, RT-qPCR for downstream targets, and flow cytometry for receptor surface expression. Functional assays such as cell migration, invasion, cytokine ELISA (IL-4, IL-5, IL-13), and co-immunoprecipitation with ACT1 can dissect signaling pathways. In vivo xenograft studies assess tumor growth and metastasis. These cells are suitable for screening inhibitors of the IL17RB-ACT1 interaction and investigating drug resistance. For further information, contact Ascent Research.
