The IL11 Knockout 786-O Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human 786-O renal cell carcinoma line. This model features targeted disruption of the IL11 gene, which encodes interleukin-11, a multifunctional cytokine implicated in hematopoiesis, inflammation, and fibrosis. The polyclonal format comprises a heterogeneous cell population bearing diverse loss-of-function edits at the endogenous locus, preserving cellular diversity while enabling robust functional genomics studies. This knockout tool provides researchers with a powerful system to interrogate IL11-dependent signaling in a cancer-relevant context.
The parental 786-O cell line originates from a clear cell renal cell carcinoma and serves as a widely used epithelial cancer model. These cells exhibit aggressive growth characteristics and mesenchymal features, rendering them suitable for investigations of tumor progression, invasion, and metastasis. The clear cell renal carcinoma background, often associated with VHL inactivation and HIF pathway dysregulation, offers a clinically pertinent environment for examining the contributions of IL11 to renal oncogenesis and stromal remodeling.
Interleukin-11 signals through a receptor complex composed of IL11RA and the gp130 co-receptor. Ligand engagement triggers activation of receptor-associated JAK1 and JAK2 tyrosine kinases, which in turn phosphorylate and activate STAT3 transcription factor. Phosphorylated STAT3 translocates to the nucleus and promotes expression of target genes such as SOCS3, BCL2, collagen, and fibronectin. Additionally, IL11 stimulation recruits SHP2 and GRB2 adaptor proteins, leading to ERK/MAPK pathway activation; crosstalk with the PI3K/AKT pathway has also been documented. Upstream, IL11 expression is regulated by TGF-??1, angiotensin II, mechanical stress, and various inflammatory cytokines. Thus, IL11 integrates multiple extracellular cues to orchestrate proliferative and fibrotic transcriptional programs.
In the context of renal cell carcinoma and fibrosis, IL11 signaling contributes to tumor cell proliferation, survival, and extracellular matrix deposition. Knockout of IL11 in 786-O cells disrupts JAK/STAT3 and ERK/MAPK signaling cascades, leading to diminished expression of downstream effectors such as STAT3, collagen, and fibronectin. This loss-of-function model is therefore invaluable for dissecting the specific roles of IL11 in driving cancer cell-intrinsic malignant properties and modulating tumor?Cstroma interactions. By abolishing IL11-mediated signal transduction, researchers can assess the impact on fibrotic responses and tumorigenic potential.
This polyclonal knockout cell population is suited for a broad range of experimental applications. In renal cell carcinoma research, it can be used to study IL11-dependent proliferation, migration, and invasion via standard techniques including western blotting, RT-qPCR, and proliferation assays. For fibrosis studies, phospho-STAT3 analysis, migration/invasion assays, and RNA-seq can delineate IL11-driven fibrogenic signaling networks. The model also facilitates drug resistance investigations and global transcriptomic profiling. For further information or to inquire about this product, please contact Ascent Research.
