The IL17RB Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human SK-OV-3 ovarian adenocarcinoma cells with targeted disruption of the IL17RB gene. This product provides a loss-of-function model system for investigating interleukin-17 receptor B (IL-17RB) signaling in a relevant ovarian cancer background. The polyclonal knockout population, derived from SK-OV-3 epithelial cells, retains the heterogeneity of the original cell line while abolishing functional expression of IL-17RB, enabling robust examination of its role in tumor biology.
SK-OV-3 cells are human ovarian adenocarcinoma epithelial cells originally isolated from the ascitic fluid of a patient with advanced ovarian cancer. This cell line is extensively employed as a model for high-grade serous ovarian carcinoma, the most common and lethal subtype of the disease. SK-OV-3 cells exhibit characteristic epithelial morphology in culture and are known for their utility in studies of ovarian tumorigenesis, chemoresistance, and the tumor microenvironment. The ascites-derived origin of these cells reflects the peritoneal dissemination typical of ovarian cancer progression, making them particularly suitable for research into metastatic mechanisms and inflammatory signaling pathways that contribute to disease aggressiveness.
IL17RB encodes a receptor for the cytokines IL-17B and IL-25 (IL-17E), which are implicated in pro-inflammatory and tumor-promoting processes. Upon ligand engagement, IL-17RB recruits the adaptor proteins ACT1 and TRAF6, which together with TAB2 facilitate activation of the kinase TAK1. TAK1 subsequently phosphorylates and activates the IKK complex and mitogen-activated protein kinases (MAPKs), triggering downstream signaling cascades. This results in the nuclear translocation of transcription factors NF-??B and AP-1, which promote the expression of a range of pro-inflammatory and oncogenic mediators, including IL-6, IL-8, TNF-??, and various chemokines. Knockout of IL17RB in this model disrupts the entire signaling axis, preventing ligand-induced activation of these pathways and providing a clean background for dissecting IL-17RB-dependent functions.
In the context of ovarian cancer, IL-17RB signaling has been implicated in promoting tumor cell proliferation, survival, migration, and chemoresistance, as well as in shaping a pro-tumorigenic inflammatory milieu. The SK-OV-3 cell line, representing high-grade serous ovarian carcinoma, provides an appropriate host to investigate these mechanisms. By employing this polyclonal IL17RB knockout population, researchers can assess the contribution of IL-17RB to key malignant properties in a heterogeneous cell population that more closely mirrors the genetic and phenotypic diversity of tumors. This model enables the discrimination of IL-17RB-dependent effects from other redundant or parallel signaling events, facilitating precise evaluation of its role in ovarian cancer pathogenesis.
This knockout model is suitable for a wide range of experimental applications, including interrogation of IL-17 signaling in ovarian cancer, analysis of tumor-stroma interactions, and validation of IL17RB as a potential therapeutic target. Researchers can utilize this system for mechanistic studies employing techniques such as western blotting and RT-qPCR to confirm gene expression changes, Sanger sequencing to verify knockout status, and luciferase reporter assays to measure NF-??B transcriptional activity. Functional assays including cytokine ELISA (for IL-6 and IL-8), phospho-signaling analysis of p-p65 and p-ERK, cell proliferation and migration/invasion assays, and drug sensitivity profiling are all readily performed with these cells. The polyclonal nature of the knockout population supports population-level analyses that account for cellular heterogeneity inherent to cancer. For further information or technical support, please contact Ascent Research.
