The IL11 Knockout LoVo Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human LoVo colorectal adenocarcinoma cell line, with targeted disruption of the IL11 gene. This loss-of-function model enables investigation of IL11-dependent signaling pathways in a cancer-relevant context, free from clonal selection biases inherent in single-cell-derived clones.
The LoVo parental cell line was established from a metastatic left supraclavicular lymph node of a 56-year-old Caucasian male with colon adenocarcinoma. These epithelial cells are tumorigenic in nude mice and exhibit molecular hallmarks including microsatellite instability (MSI-H), CpG island methylator phenotype-high (CIMP-high), and a BRAF V600E mutation. This genetic background makes LoVo a robust model for studying oncogenic signaling, chemoresistance, and metastatic progression in colorectal adenocarcinoma.
IL11 is a pleiotropic cytokine that signals via a receptor complex composed of IL11RA and gp130 (IL6ST), leading to JAK-mediated phosphorylation and nuclear translocation of STAT3. Activated STAT3 transcriptionally upregulates genes driving cell cycle progression (CCND1), survival (BCL2L1), extracellular matrix remodeling (MMP9), and angiogenesis (VEGF). The pathway is stimulated by upstream regulators including TGF-beta, IL-1, and Oncostatin M, and is restrained by the feedback inhibitor SOCS3. IL11 also engages the MAPK/ERK and PI3K/AKT cascades, broadening its impact on cellular proliferation, differentiation, and stress responses.
In LoVo colorectal cancer cells, autocrine IL11/STAT3 signaling contributes to malignant phenotypes such as apoptosis resistance, enhanced proliferation, and increased metastatic capacity. The presence of a BRAF V600E mutation and MSI-H status creates a unique dependency on cytokine-driven survival networks, where IL11 may cooperate with TGF-beta to promote epithelial-mesenchymal transition and fibrotic responses. Disrupting IL11 in this polyclonal population allows researchers to interrogate how loss of IL11 alters the activity of key downstream mediators like STAT3, BCL2L1, and MMP9, and to evaluate compensatory signaling rewiring.
This knockout product is ideal for functional genomics and drug discovery applications. Common readouts include western blotting for phosphorylated and total STAT3, RT-qPCR or transcriptomic profiling via RNA-seq, and cell viability assays such as MTS or colony formation. Migration and invasion capabilities can be assessed using Boyden chamber or wound healing assays, with apoptosis measured by Annexin V/PI flow cytometry. Broader pathway analysis can be performed using phospho-kinase arrays and cytokine multiplex assays to map signaling alterations upon IL11 disruption. These approaches support studies ranging from target validation of IL11 pathway inhibitors to mechanism-of-action research. For additional product information, please contact Ascent Research.
