The IL11 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the T-47D human breast ductal carcinoma cell line, designed to disrupt the IL11 gene. This polyclonal format encompasses a collection of cells with heterogeneous loss-of-function mutations at the target locus, offering a population-level ablation of interleukin-11 that minimizes clonal selection bias and ensures robust, reproducible functional studies.
The parental T-47D cell line, established from a pleural effusion of a mammary ductal carcinoma, is a widely recognized luminal A breast cancer model. It is estrogen receptor (ER)-positive and progesterone receptor (PR)-positive and exhibits strong estrogen responsiveness, retaining critical features of hormone-dependent tumor biology. Its well-characterized genomic background and stable epithelial phenotype facilitate investigation of oncogenic signaling and therapeutic resistance mechanisms.
Interleukin-11 is a pleiotropic cytokine that initiates signaling by binding to its specific receptor subunit IL11RA and the common signal transducer gp130 (IL6ST). Ligand engagement activates receptor-associated Janus kinases JAK1 and JAK2, leading to phosphorylation and nuclear translocation of STAT3, as well as stimulation of the RAS-MAPK cascade and the PI3K-AKT1 axis. This pathway is subject to regulation by upstream factors such as TGFB1, IL1B, and oncogenic RAS. Downstream effectors like STAT3, AKT1, MAPK1, CCND1, and BCL2 coordinate cellular responses including proliferation, survival, and migratory capacity, while the suppressor SOCS3 provides negative feedback control.
In the T-47D luminal A context, IL11 knockout provides a powerful tool to dissect the interplay between gp130 cytokine signaling and estrogen receptor pathways. IL11 overexpression is implicated in breast cancer bone metastasis by driving osteoclastogenesis and modifying the tumor microenvironment. Moreover, IL11-mediated activation of STAT3 and AKT1 promotes epithelial-mesenchymal transition and resistance to endocrine and chemotherapeutic agents, making this model valuable for studying aggressive disease features and therapeutic vulnerabilities.
These polyclonal knockout cells are suited for a variety of experimental applications, including MTT-based proliferation assays, transwell migration/invasion studies, phospho-STAT3 flow cytometry, western blotting, RT-qPCR, and RNA-seq. They enable co-culture systems to model tumor-osteoclast interactions and high-throughput compound screens targeting the IL11-gp130 axis. For additional information or to place an order, please contact Ascent Research.
