The CCL7 Knockout MCF-7 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MCF-7 human breast adenocarcinoma cell line, engineered for disruption of the CCL7 gene. This polyclonal knockout model provides a powerful loss-of-function system for investigating the biological roles of the chemokine CCL7, particularly in the context of tumor?Cimmune interactions and breast cancer progression. By targeting CCL7, researchers can dissect its contributions to chemotactic signaling and downstream inflammatory pathways without relying on pharmacological inhibition, enabling robust functional genomics studies in a well-characterized epithelial background.
The host MCF-7 cell line is an estrogen receptor-positive, luminal A subtype mammary adenocarcinoma model originally isolated from the pleural effusion metastasis of a 69-year-old Caucasian female. Its epithelial origin, hormone responsiveness, and widespread adoption in cancer biology make it particularly suitable for studying chemokine networks that influence tumor cell motility, invasion, and crosstalk with the microenvironment. The polyclonal knockout pool retains the key characteristics of the parental line while introducing targeted CCL7 deficiency, offering a genetically defined tool for metastasis and immunomodulation research.
CCL7 (monocyte chemotactic protein-3) is a chemokine that orchestrates the recruitment of monocytes, eosinophils, and basophils to inflammatory sites and the tumor microenvironment. Its expression is transcriptionally regulated by upstream activators including TNF-??, IL-1??, NF-??B, and STAT3. Following secretion, CCL7 binds to the chemokine receptors CCR1, CCR2, and CCR3, which are coupled to G proteins and trigger intracellular cascades involving phospholipase C (PLC) and protein kinase C (PKC). These events converge on the MAPK and PI3K-AKT pathways, driving cytoskeletal rearrangements and cell migration. The knockout disrupts this chemotactic gradient, impairing receptor-mediated signaling and ablating the downstream effector mechanisms that normally facilitate immune cell trafficking and pro-metastatic inflammation.
In the MCF-7 context, CCL7 ablation is particularly relevant for dissecting the paracrine loops between tumor cells and infiltrating leukocytes that fuel breast cancer invasion and metastasis. Since MCF-7 cells express functional CCR2 and respond to autocrine chemokine signaling, the CCL7 knockout model eliminates a key driver of monocyte/macrophage recruitment and the associated production of tumor-promoting factors. This polyclonal population allows researchers to examine how loss of CCL7 alters tumor sphere formation, matrix degradation, and metastatic potential, while avoiding clonal artifacts. It also facilitates investigation of compensatory mechanisms within the broader chemokine network.
This knockout cell tool is suited for diverse applications, including the study of chemokine-mediated immune cell recruitment in breast cancer, evaluation of tumor microenvironment interactions, metastasis research, and drug target validation along the CCL7/CCR axis. Researchers can validate CCL7 knockout via Western blotting, RT-qPCR, or ELISA, and perform functional assays such as Transwell migration, chemotaxis, and co-culture experiments with immune cells. Tumor sphere formation assays provide additional readouts of cancer stem cell-like properties. For further details on product specifications, lot-to-lot consistency, or custom engineering requests, please contact Ascent Research.
