IL11 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human epithelial cell line. This heterogeneous pool carries targeted disruption of the IL11 gene, providing a loss-of-function model for studying IL-11-dependent processes. The polyclonal nature retains genetic diversity, enabling investigation in a mixed cellular background. These gene-edited cells are suitable for a range of functional assays and require appropriate validation of knockout efficiency in polyclonal populations.
The CAL-27 cell line was established from a poorly differentiated squamous cell carcinoma of the tongue and serves as a model for head and neck squamous cell carcinoma (HNSCC). These adherent epithelial cells exhibit rapid proliferation and invasive potential, characteristic of aggressive oral cancers. Widely used in oral cancer research, CAL-27 provides a clinically relevant platform to dissect oncogenic signaling. This knockout model in the CAL-27 background enables direct interrogation of IL-11’s role in HNSCC pathogenesis.
Interleukin-11 (IL-11) signals through IL11RA and gp130/IL6ST, recruiting JAK1/2 to phosphorylate STAT3. Activated STAT3 drives transcription of BCL2, CCND1, MYC, MMP2, and MMP9, promoting survival, proliferation, and invasion. IL-11 also activates MAPK/ERK (via ELK1 and FOS) and PI3K-AKT pathways, enhancing tumorigenic phenotypes. Key upstream regulators include TGFB1, IL1B, TNF, EGF, and PDGF, while SOCS3 provides negative feedback on JAK/STAT signaling.
In CAL-27 cells, IL-11 drives aggressive HNSCC behavior by promoting STAT3-dependent transcription of pro-survival and pro-migratory genes, contributing to tumor growth, metastasis, and therapy resistance. Disrupting IL11 allows dissection of its specific roles in oncogenic signaling, matrix remodeling, and immune evasion. The polyclonal nature preserves cellular heterogeneity, making it valuable for studying tumor microenvironment interactions and IL-11-mediated cancer cell plasticity.
This knockout model is suited for functional analysis of JAK/STAT, MAPK/ERK, and PI3K-AKT pathways in oral cancer. Representative assays include western blotting for p-STAT3, RT-qPCR of IL11 targets, transwell migration/invasion, MTT/colony formation, and flow cytometry for apoptosis. Co-immunoprecipitation can probe gp130 interactions, and RNA-seq enables transcriptomic profiling. The model facilitates studies of cytokine-mediated drug resistance and tumor-stroma crosstalk. For further information, please contact Ascent Research.
