The IL11 Knockout MCF-7 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of MCF-7 human breast adenocarcinoma epithelial cells carrying targeted disruptions of the IL11 gene. This knockout model abolishes IL11 expression without clonal isolation, providing a heterogeneous loss-of-function background ideal for studying IL11-dependent signaling. Derived from an estrogen receptor-positive line, these cells maintain key characteristics of the parental MCF-7, enabling functional interrogation in a well-defined oncogenic context. The polyclonal format avoids clonal selection bias and supports robust, reproducible studies.
MCF-7 is an adherent epithelial cell line derived from the pleural effusion of a metastatic breast adenocarcinoma patient, predominantly used as a model for luminal A breast cancer. These cells express estrogen receptor alpha and are dependent on estrogen for proliferation, retaining differentiated features such as cytokeratin expression and junction formation. MCF-7 exhibits low basal invasiveness but can undergo epithelial-mesenchymal transition upon cytokine stimulation. This well-characterized background provides a platform for dissecting how IL11 contributes to hormone-responsive breast cancer progression.
IL11 is a pleiotropic cytokine that signals via the IL11RA/gp130 heterodimer, activating JAK1 to phosphorylate STAT3, and concurrently engaging MAPK/ERK and PI3K/AKT cascades. Upstream regulators include TGFB1, IL1B, TNF, mechanical stretch, and hypoxia. Downstream, IL11 transcriptionally modulates targets such as CCND1, BCL2, MMP9, and SOCS3, effecting changes in proliferation, survival, motility, and matrix remodeling. This network positions IL11 at the intersection of inflammation, fibrosis, and cancer.
In ER-positive breast adenocarcinoma, gp130 cytokines like IL11 can influence tumor cell-autonomous traits and the surrounding microenvironment. IL11 may promote cancer cell proliferation and survival, while also activating fibroblasts to foster a protumorigenic stroma. The IL11 knockout MCF-7 model allows dissection of these effects, enabling assessment of whether IL11 loss attenuates malignant phenotypes or alters therapeutic sensitivities. This tool is valuable for exploring IL11 as a target in breast cancer and fibrotic complications.
Typical applications include western blotting for phospho-STAT3 and phospho-ERK1/2, RT-qPCR for IL11 transcriptional targets, and functional assays such as MTS proliferation, wound healing migration, and transwell invasion. Apoptosis analysis by annexin V staining reveals dependencies on survival signals. These cells are amenable to co-culture with fibroblasts to study paracrine loops and to screening of JAK/STAT or gp130 inhibitors. For further details, please contact Ascent Research.
