The IL11 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma HT29 cell line, featuring CRISPR/Cas9-mediated disruption of the interleukin-11 (IL11) gene. This polyclonal population, generated without single-cell cloning, provides a loss-of-function model system to investigate IL11-dependent signaling and cellular phenotypes in a well-characterized intestinal epithelial context. The heterogeneous pool of edited cells reflects the diversity of individual knockout events, enabling robust and reproducible study of IL11 function while avoiding clonal variation artifacts.
HT29 cells originate from a human colorectal adenocarcinoma and display an epithelial morphology with a BRAF V600E mutation and microsatellite-stable (MSS) status. These cells are widely used as a model of intestinal epithelial biology, possessing the capacity for enterocytic differentiation and tumorigenic potential, making them particularly relevant for colorectal cancer research. Their molecular profile and experimental tractability support the study of oncogenic signaling, cytokine responsiveness, and tumor?Cstroma interactions.
IL11 encodes a pleiotropic cytokine that signals through the IL11RA/gp130 receptor complex, primarily activating the JAK/STAT3 pathway and additionally engaging MAPK/ERK and PI3K/AKT cascades. Upstream, IL11 expression is induced by factors such as TGF-??, IL-1??, and TNF-??, acting via NF-??B and STAT3. Upon receptor engagement, IL11 stimulates JAK1 and JAK2 kinases, leading to STAT3 phosphorylation and transcription of downstream targets including CCND1, BCL2, BIRC5, VEGFA, and MMP9, thereby promoting cell cycle progression, survival, angiogenesis, and matrix remodeling.
In the context of HT29 colorectal cancer cells, IL11 contributes to tumor-promoting processes, including enhanced proliferation, survival, migration, and metastatic potential, largely through STAT3-driven transcriptional programs. Disruption of IL11 in this polyclonal knockout model allows researchers to dissect its specific contributions to malignant phenotypes, evaluate compensatory mechanisms, and validate IL11 as a therapeutic target. The MSS/BRAFV600E background adds clinical relevance, as it resembles a distinct molecular subtype of colorectal carcinoma with limited treatment options.
Typical applications include quantifying the impact of IL11 loss on STAT3 phosphorylation and target gene expression by Western blotting and RT-qPCR, assessing proliferation via MTT assays, measuring migration using transwell chambers, and monitoring secreted IL11 levels by ELISA. The model further supports xenograft tumor growth studies to evaluate in vivo tumorigenicity and therapeutic response, as well as apoptosis assays (e.g., Annexin V staining) to probe IL11-dependent survival signals. These polyclonal HT29 IL11 knockout cells are a valuable resource for cancer biology, inflammation research, and drug discovery programs. For further information and ordering details, please contact Ascent Research.
