The IL11 Knockout HCT 116 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of the HCT 116 colorectal carcinoma cell line with targeted disruption of the IL11 gene. This knockout model is designed to ablate functional interleukin-11 (IL11) expression through gene editing, yielding a heterogeneous mixture of cells each carrying distinct editing outcomes. The polyclonal format offers a robust loss-of-function background without the need for single-cell cloning, facilitating scalable and reproducible experiments. These cells are optimized for investigating IL11-mediated processes in a cancer-relevant system.
The HCT 116 host cell line is a well-characterized human colorectal carcinoma model harboring an oncogenic KRAS G13D mutation, high microsatellite instability (MSI-high), and wild-type p53 status. These genetic features render HCT 116 cells particularly valuable for studying colorectal cancer progression and therapeutic responses. The cell line retains epithelial morphology and is widely employed in xenograft models and in vitro assays. Its MSI-high phenotype also makes it relevant for immuno-oncology research, as it mimics a subset of colorectal tumors with elevated mutational burden.
IL11 is a pleiotropic cytokine of the IL-6 family that signals via a heterodimeric receptor composed of IL11RA and gp130 (IL6ST). Binding activates associated JAK1 and JAK2 kinases, leading to phosphorylation of STAT3 and stimulation of the MAPK/ERK pathway through ERK1/2. Downstream transcriptional targets include BCL2L1, CCND1, and profibrotic genes such as COL1A1 and ACTA2. Expression of IL11 is induced by TGF-??, IL-1, and TNF-??, positioning it as a critical integrator of inflammatory and fibrogenic signals. Consequently, IL11 promotes fibrosis, cell survival, and proliferation in multiple disease contexts.
Disruption of IL11 in HCT 116 cells is expected to impair STAT3- and ERK1/2-dependent signaling, attenuating fibrotic and tumorigenic phenotypes. The colorectal carcinoma origin of the host line, combined with its KRAS G13D mutation and MSI-high status, provides a relevant milieu for assessing IL11??s role in inflammation-associated cancer progression. This model enables investigation of potential synergies or antagonisms between mutant KRAS-driven MAPK signaling and IL11-mediated pathways, offering insights into combinatorial therapeutic strategies.
These polyclonal knockout cells support diverse experimental workflows, including phospho-STAT3 western blotting, RT-qPCR analysis of IL11 and its downstream effectors, cell proliferation and colony formation assays, and RNA-seq transcriptomics. They are ideal for high-throughput screening of IL11RA/gp130 inhibitors and for dissecting TGF-??-induced fibrotic responses. Additionally, the model facilitates studies on the interplay between inflammatory signals and oncogenic pathways in colorectal cancer. For further details, please contact Ascent Research.
