The CCL7 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D breast carcinoma line. This product features a mixed pool of cells bearing targeted disruptions in the CCL7 locus, eliminating functional CCL7 expression without clonal isolation. The polyclonal format provides a representative loss-of-function model while maintaining cellular heterogeneity, making it suitable for assays that require population-level analysis of chemokine signaling disruption.
The T-47D cell line originates from the pleural effusion of a patient with invasive ductal carcinoma and displays estrogen and progesterone receptor positivity (ER+/PR+). As a well-established model of hormone-responsive breast cancer, it recapitulates key features of luminal A tumor biology, including dependence on endocrine signaling pathways. This line is extensively used to study tumor-stroma interactions, therapeutic responses, and the immunomodulatory roles of epithelial-derived factors within the tumor microenvironment.
CCL7 (MCP-3) is a potent chemoattractant for monocytes and lymphocytes, induced by TNF-??, IL-1, and interferon-?? via NF-??B and STAT3 activation. Secreted CCL7 engages the chemokine receptors CCR1, CCR2, and CCR3, triggering G-protein-dependent signaling cascades. Downstream, it phosphorylates MAPK1/3 and AKT via the Ras/Raf pathway and activates JAK2/STAT3 and NF-??B, ultimately enhancing MMP9 expression and leukocyte migration. The knockout disrupts these signaling axes, eliminating CCL7-mediated PI3K/AKT and JAK/STAT transduction and halting chemotactic responses.
In T-47D breast cancer cells, CCL7 functions as a key paracrine mediator that recruits tumor-associated macrophages, contributing to an immunosuppressive and angiogenic microenvironment. By ablating CCL7, researchers can directly assess the impact on monocyte chemotaxis and downstream pathways that intersect with ER signaling, including PI3K/AKT-driven survival and JAK/STAT-mediated cytokine feedback loops. This model is instrumental for dissecting how inflammatory chemokine networks modulate hormone-responsive tumor progression and resistance mechanisms.
The polyclonal knockout cells are designed for diverse experimental platforms, including transwell chemotaxis assays to measure monocyte migration, Western blotting for phospho-AKT and phospho-STAT3 analysis, and RT-qPCR arrays for cytokine profiling. They support proliferation and migration studies, flow cytometric assessment of receptor expression, and high-content screening of CCL7 pathway inhibitors. For bespoke technical support, contact Ascent Research.
