The IL17RB Knockout T-47D Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the IL17RB gene has been disrupted to generate a loss-of-function model. This polyclonal pool is derived from the human breast cancer cell line T-47D and provides a heterogeneous collection of edited alleles, enabling functional studies of IL17RB without clonal bias. The knockout eliminates IL17RB protein expression, thereby abrogating receptor-mediated signaling downstream of its ligands IL17B and IL25.
The T-47D host cell line was established from the pleural effusion of a ductal carcinoma and serves as a widely used model of estrogen receptor-positive (ER+) breast cancer. These cells retain key characteristics of luminal A breast cancer, including expression of estrogen and progesterone receptors, and are commonly employed to investigate hormone-dependent and -independent pathways in breast tumor biology. The use of T-47D as the host enables dissection of IL17RB function specifically within the ER+ breast cancer subtype.
IL17RB encodes a receptor that, upon binding its ligands IL17B or IL25 (IL17E), forms a heterodimeric complex with IL17RA. The activated receptor recruits the adaptor protein ACT1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6, triggering downstream pathways including NF-??B and the MAP kinases ERK, JNK, and p38. These cascades promote the transcription of pro-inflammatory mediators such as IL-6, IL-8, and CXCL1, as well as anti-apoptotic genes. Additionally, JAK-STAT signaling can contribute to IL17RB-mediated transcriptional responses. This signaling network positions IL17RB at the intersection of inflammatory and oncogenic processes.
In the context of ER+ breast cancer, IL17RB has been implicated in promoting tumor progression, metastasis, and immune evasion through its pro-inflammatory and pro-survival effects. Disruption of IL17RB in T-47D cells allows researchers to directly assess its role in modulating cancer cell proliferation, migration, and response to cytokine stimulation. Because T-47D cells express estrogen receptors, this knockout model also provides a platform to explore crosstalk between IL17RB signaling and endocrine pathways, potentially revealing new targets for therapeutic intervention in hormone-responsive breast cancers.
Typical applications include functional characterization of IL17B/IL25 signaling, drug target validation, and immunomodulation studies. Western blotting confirms IL17RB knockout, while RT-qPCR, MTT, Transwell, NF-??B reporter, and ELISA assays examine downstream signaling and functional consequences. RNA-seq and flow cytometry enable transcriptomic and phenotypic profiling. This polyclonal knockout population is a versatile tool for cancer biology and inflammation research. For further information, please contact Ascent Research.
