The CCL7 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-OV-3 human ovarian adenocarcinoma line. This product features targeted disruption of the CCL7 gene, eliminating monocyte chemotactic protein-3 (MCP-3) expression. The polyclonal format represents a heterogeneous loss-of-function model, avoiding clonal selection artifacts and enabling the study of bulk cellular responses. It provides a versatile system for investigating chemokine-mediated processes in ovarian cancer research.
The parental SK-OV-3 cell line is derived from the ascites of a 64-year-old Caucasian female with ovarian adenocarcinoma. It exhibits a hypertriploid karyotype and is null for the tumor suppressor p53, while expressing the receptor tyrosine kinases EGFR and HER2. These characteristics render SK-OV-3 a well-established model for studying advanced ovarian cancer, particularly for mechanisms of metastasis, ascites formation, and therapeutic resistance. The cells are adherent and form tumors in xenograft models, recapitulating key aspects of the human disease microenvironment.
CCL7 encodes MCP-3, a CC chemokine that recruits monocytes, eosinophils, basophils, dendritic cells, and activated T cells via chemokine receptors CCR1, CCR2, CCR3, and CCR5, as well as the atypical receptor ACKR1 (DARC). Ligand binding activates Gi proteins, leading to PLC-mediated IP3 and DAG production, calcium mobilization, and downstream activation of PI3K-AKT and MAPK/ERK cascades, along with Rho GTPase-driven actin polymerization. CCL7 expression is induced by TNF-alpha, IL-1beta, IFN-gamma, and LPS through NF-kappaB, STAT1, and AP-1 transcription factors. In the tumor microenvironment, MCP-3 promotes leukocyte infiltration, fueling chronic inflammation and tumor progression.
In SK-OV-3 cells, CCL7 knockout abrogates MCP-3 secretion, impairing CCR1/2/3/5-mediated chemotaxis of myeloid cells and T lymphocytes, thereby reducing tumor-associated inflammation. This is critical in ovarian cancer, where malignant ascites formation depends on chemokine-driven vascular permeability and immune trafficking. The model helps delineate CCL7’s role in peritoneal metastasis and immunosuppressive niche development.
These polyclonal knockout cells are suitable for transwell migration assays to measure monocyte/T cell chemotaxis, ELISA for MCP-3 quantification, and qPCR/western blotting for signaling analysis. They can be used in invasion assays and xenograft models to study metastasis and ascites, and for screening anti-metastatic compounds or immunotherapies. For technical inquiries, please contact Ascent Research.
