CCL7 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human CCL7 gene in the LoVo colorectal adenocarcinoma cell line. This heterogeneous pool of gene-disrupted cells provides a loss-of-function model suitable for population-level studies of chemokine signaling, without the biases of clonal selection. The product is designed for robust functional assays where ablation of CCL7-mediated pathways is required in a metastatic colorectal cancer background.
The LoVo cell line, derived from a metastatic colon adenocarcinoma, is a well-established model for colorectal cancer research, particularly for invasion, metastasis, and tumor?Cmicroenvironment interactions. It retains epithelial morphology and key oncogenic signaling networks, offering a reliable platform for genetic manipulation and downstream phenotypic analyses such as chemotaxis and proliferation assays.
CCL7 encodes monocyte chemoattractant protein-3 (MCP-3), a CC chemokine that binds the receptors CCR1, CCR2, and CCR3. Ligand engagement activates G-protein-coupled signaling cascades involving PI3K-AKT and MAPK pathways, leading to calcium mobilization and cytoskeletal rearrangements that drive cell migration. CCL7 expression is induced by pro-inflammatory stimuli such as TNF-alpha, IL-1, and IFN-gamma through NF-kB and STAT3, while downstream effectors include MAPK1/3, AKT, and Rho GTPases. Interactions with glycosaminoglycans and the atypical receptor DARC modulate chemokine availability and gradient formation.
In LoVo cells, CCL7 contributes to autocrine and paracrine signaling loops that promote tumor cell chemotaxis and invasiveness. Knockout of CCL7 is predicted to impair monocyte chemotaxis and attenuate immune cell recruitment-driven metastatic progression. This model is directly relevant to colorectal cancer metastasis, inflammatory bowel disease, and other pathologies where chemokine-mediated leukocyte trafficking is critical for disease progression.
Typical applications encompass tumor microenvironment studies, colorectal cancer metastasis research, chemokine pathway analysis, and drug target validation. Compatible assays include Transwell migration and monocyte chemotaxis assays, RT-qPCR, western blotting, flow cytometry, cell proliferation assays, and co-culture with immune cells. These polyclonal knockout cells enable detailed dissection of the CCL7?CCCR signaling axis and its role in tumor cell invasiveness. For further technical information or ordering inquiries, please contact Ascent Research.
