The CCL7 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human lung squamous cell carcinoma cell line. This product offers a heterogeneous pool of cells with targeted disruption of the CCL7 gene, enabling loss-of-function studies without the need for single-cell cloning. The pooled format preserves the genetic diversity of the knockout model, reducing clonal artifacts while providing a robust system for investigating CCL7-dependent phenotypes in a relevant cancer background.
NCI-H1703 is a well-established human lung squamous cell carcinoma cell line originally derived from a primary lung tumor. This adherent cell line is widely employed as an in vitro model of non-small cell lung cancer, particularly for studying the molecular mechanisms of lung carcinogenesis, tumor-stroma interactions, and therapeutic resistance. Its squamous cell carcinoma origin makes it especially valuable for dissecting pathways that drive malignancy and metastasis in this histological subtype, which accounts for a significant proportion of lung cancer cases.
CCL7 (MCP-3) is a secreted chemokine that functions as a potent chemoattractant for monocytes, eosinophils, basophils, and dendritic cells. It exerts its biological effects by binding to chemokine receptors CCR1, CCR2, and CCR3, which are G-protein-coupled receptors. Upon ligand binding, these receptors activate downstream signaling cascades including MAPK/ERK and PI3K/Akt pathways, as well as JAK-STAT and NF-??B signaling modules. Upstream, CCL7 expression is transcriptionally regulated by pro-inflammatory cytokines such as TNF-??, IL-1??, and IFN-??, often via NF-??B and AP-1 transcription factors. Downstream effects include integrin activation, induction of matrix metalloproteinases, and modulation of adhesion molecules, collectively promoting directed cell migration and tissue remodeling. Additionally, CCL7 interacts with glycosaminoglycans on cell surfaces and the extracellular matrix, which helps establish chemotactic gradients.
In the NCI-H1703 background, loss of CCL7 expression allows researchers to dissect the autocrine and paracrine roles of this chemokine in lung squamous cell carcinoma progression. Since CCL7 is implicated in recruiting immune cells to the tumor microenvironment and promoting angiogenesis, this knockout model enables the study of how tumor-derived CCL7 influences the inflammatory milieu and metastatic potential. The polyclonal nature of the knockout cells ensures that subsequent functional analyses, such as invasion and migration assays, reflect a population-level response rather than clonal idiosyncrasies. This makes the model particularly suitable for drug target validation and for examining crosstalk between cancer cells and stromal components.
Typical applications include chemotaxis assays using Boyden chambers to evaluate migration, ELISA and RT-qPCR to quantify CCL7 secretion and expression, western blotting for pathway activation, and flow cytometry to assess receptor expression. Co-culture systems can be employed to investigate immune cell recruitment, while immunofluorescence and co-immunoprecipitation facilitate protein interaction studies. Phospho-signaling analysis allows mapping of CCL7-dependent kinase cascades. This product serves as a versatile tool for exploring CCL7??s role in lung cancer, inflammation, and angiogenesis, and for identifying novel therapeutic targets. For further technical specifications or custom inquiries, please contact Ascent Research.
