The IL17RB Knockout MCF-7 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population, generated through targeted disruption of the IL17RB gene in the MCF-7 human breast adenocarcinoma cell line. This polyclonal product provides a heterogeneous loss-of-function model, enabling researchers to interrogate IL-17RB-dependent signaling pathways without confounding clonal artifacts. The knockout cells are designed for rigorous in vitro studies of cytokine receptor biology, immune modulation, and breast cancer progression, serving as a versatile tool for target validation and mechanistic dissection.
MCF-7 is an epithelial cell line originally isolated from the pleural effusion of a patient with metastatic breast cancer. This cell line is characterized by expression of estrogen receptor (ER) and progesterone receptor (PR), while lacking amplification of human epidermal growth factor receptor 2 (HER2). Representing the luminal A molecular subtype, MCF-7 cells retain key hormone-responsive signaling networks and are widely employed as a model system for hormone receptor-positive breast cancer. The well-documented genetic background and standardized culture conditions of MCF-7 make it particularly suitable for knockout studies aimed at understanding gene function in a clinically relevant tumor context.
IL17RB encodes a subunit of the heterodimeric receptor complex for interleukin-25 (IL-25, also known as IL-17E) and IL-17B. Upon ligand engagement, IL-17RB pairs with IL-17RA, leading to the recruitment of the adaptor protein Act1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6. This molecular assembly triggers downstream activation of the canonical NF-??B and MAPK/ERK cascades, culminating in the transcriptional induction of Th2-associated cytokines such as IL-4, IL-5, and IL-13, as well as chemokines including CCL2 and CXCL1. Upstream regulators of this axis include the transcription factors GATA3 and STAT6, which integrate environmental cues into IL-17RB expression and function.
In the context of MCF-7 cells, IL-17RB signaling may intersect with estrogen receptor pathways to influence cell proliferation, survival, and invasive capacity. The knockout model facilitates the dissection of IL-17RB-mediated contributions to tumor cell-autonomous phenotypes and paracrine interactions within the tumor microenvironment. By eliminating IL-17RB expression, researchers can assess the dependency of hormone receptor-positive breast cancer cells on IL-25-driven signaling, thereby evaluating the receptor’s potential as a therapeutic target in a subtype-specific manner.
This polyclonal knockout product enables a broad range of experimental approaches, including western blotting for phospho-NF-??B and phospho-ERK, RT-qPCR profiling of IL-4, IL-13, and chemokine expression, flow cytometric determination of IL-17RB surface levels, cell proliferation and apoptosis assays, and functional migration/invasion studies. Additional applications comprise co-immunoprecipitation of the IL-17RB/IL-17RA complex and NF-??B luciferase reporter assays. These tools support investigations into IL-17RB signaling in breast cancer biology, Th2 immune modulation in the tumor microenvironment, and therapeutic targeting of the IL-25/IL-17RB axis. For further details or inquiries, please contact Ascent Research.
