The CCL7 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal human cell population in which the gene encoding C-C motif chemokine ligand 7 (CCL7) has been disrupted. This product provides a loss-of-function model pooled from multiple edited cells, enabling the study of CCL7-dependent signaling in a heterogeneous tumor cell context without clonal selection. The polyclonal format preserves genetic diversity while ensuring target-gene knockout, making it suitable for population-level analyses of chemokine function.
These cells are derived from the CAL-27 cell line, a well-characterized human tongue squamous cell carcinoma (OSCC) epithelial model. CAL-27 cells are extensively used in oral cancer research to investigate tumor biology, metastasis, and therapeutic responses. Their epithelial origin and tumorigenic properties provide a physiologically relevant platform for dissecting the molecular mechanisms of OSCC progression, particularly the interplay between cancer cells and the immune microenvironment.
CCL7 is a potent chemoattractant for monocytes, eosinophils, and basophils, and its expression is transcriptionally regulated by pro-inflammatory cytokines such as TNF-alpha, IL-1beta, and IFN-gamma via NF-kB and AP-1 transcription factors. Secreted CCL7 binds to G-protein-coupled receptors CCR1, CCR2, and CCR3, triggering intracellular signaling cascades involving PI3K, PLC, and MAP kinases (ERK, p38), as well as JAK-STAT pathways. This signaling promotes monocyte/macrophage recruitment and induces matrix metalloproteinases (MMPs), facilitating tissue remodeling and immune cell infiltration. CCL7 also interacts with glycosaminoglycans (GAGs) on cell surfaces and extracellular matrix, enhancing its local activity.
In the context of OSCC, CCL7 contributes to an inflammatory tumor microenvironment by driving immune cell recruitment, which can support cancer progression and metastasis. Disruption of CCL7 in CAL-27 cells abolishes the autocrine and paracrine chemokine gradient, likely reducing monocyte trafficking and dampening JAK-STAT and MAPK pathway activation. This knockout model thus provides a tool to dissect the role of chemokine-mediated crosstalk between carcinoma cells and infiltrating leukocytes, and to evaluate how loss of CCL7 influences tumor aggressiveness and immune evasion.
Researchers can employ these cells in a variety of functional assays, including quantitative PCR and western blotting to validate CCL7 ablation and monitor signaling effector activation (e.g., phosphorylated STAT3 or ERK), chemotaxis and invasion assays using monocytic cell lines, and ELISA for secreted chemokine levels. Co-culture systems with peripheral blood mononuclear cells allow assessment of immune cell recruitment by flow cytometry, while drug testing experiments can explore anti-metastatic compounds targeting chemokine axes. For additional information or to request a quote, please contact Ascent Research.
