The CCL7 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human TE1 esophageal squamous cell carcinoma (ESCC) cells with targeted disruption of the CCL7 gene. This product provides a genetically heterogeneous pool of knockout cells designed for loss-of-function studies of CCL7 in a cancer epithelial context. As a polyclonal population, it avoids artifacts associated with clonal selection while maintaining efficient gene disruption, offering a robust model for analyzing chemokine function in tumor biology.
The parental TE1 cell line originates from a poorly differentiated ESCC of a male Chinese patient and serves as an established model for studying esophageal cancer progression, therapeutic resistance, and epithelial?Cstromal interactions. Its cancerous epithelial nature makes it particularly suitable for examining how chemokine secretion from tumor cells shapes the immune microenvironment and influences malignant behavior.
CCL7 encodes a CC chemokine secreted in response to inflammatory stimuli such as TNF???, IL?1??, and IFN???, acting downstream of NF???B and TLR4 signaling. Secreted CCL7 binds the chemokine receptors CCR1, CCR2, and CCR3 on monocytes, macrophages, and other leukocytes, triggering G??i?dependent signaling cascades that involve SRC, MAPK1/3 (ERK), and AKT phosphorylation. These pathways drive cytoskeletal rearrangements and directional migration, promoting leukocyte chemotaxis. Additionally, CCL7 interacts with matrix components such as glycosaminoglycans and MMP2, facilitating localized retention and remodeling of the extracellular matrix. Knockout of CCL7 interrupts these signaling axes, enabling dissection of chemokine?mediated intercellular communication.
In ESCC, CCL7 overexpression is often associated with enhanced tumor inflammation and poor prognosis. Disruption of CCL7 in TE1 cells offers a powerful tool to investigate how carcinoma?derived chemokines modulate the tumor microenvironment, including recruitment of tumor?associated macrophages and other immune cells that can support invasion and metastasis. This model is particularly valuable for studying autocrine and paracrine loops that link NF???B activation, CCL7 secretion, and CCR?dependent ERK/AKT signaling, and for evaluating how loss of CCL7 affects tumor cell invasiveness and metastatic potential.
Researchers can employ these cells in a wide range of assays to probe inflammatory signaling and tumor?immune crosstalk. Typical applications include assessing CCL7 mRNA and protein levels by RT?qPCR, ELISA, and Western blotting; measuring downstream phospho?ERK and phospho?AKT by immunoblotting; conducting monocyte migration and Matrigel invasion assays; and performing co?culture experiments with immune cells to evaluate chemotactic responses. RNA?seq and phosphoproteomic analyses can further reveal global changes in signaling networks. These polyclonal knockout cells also support compound screening for inhibitors of chemokine?mediated metastasis. For detailed technical specifications or custom services, please contact Ascent Research.
