This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line, featuring targeted disruption of the CCL7 gene (CCL7 Knockout HeLa Polyclonal Cells). The polyclonal format provides a heterogeneous pool of cells with CCL7 loss-of-function, enabling robust evaluation of chemokine-dependent processes without the limitations of clonal selection. This model is optimized for investigating the role of CCL7 in leukocyte recruitment, inflammatory signaling, and tumor biology.
The parental HeLa line is an immortalized epithelial cell line originally isolated from a HPV18-positive cervical adenocarcinoma. HeLa cells are widely employed in cancer biology, signal transduction, and pharmacology due to their robust growth, extensive molecular characterization, and suitability for functional assays. While HeLa cells do not endogenously express all immune-related pathways, they provide a tractable system to dissect CCL7-mediated signaling events relevant to cancer inflammation and cell migration.
CCL7 (monocyte chemotactic protein-3) is a CC chemokine that binds CCR1, CCR2, and CCR3 on monocytes, eosinophils, basophils, and T cells. Ligand engagement triggers G-protein-coupled receptor activation, leading to PLC-mediated IP3 and DAG production, calcium mobilization, and PKC activation. Downstream, CCL7 stimulates MAPK cascades (ERK1/2, JNK, p38), culminating in activation of transcription factors AP-1 and NF-??B and expression of pro-migratory and pro-inflammatory genes. CCL7 expression is regulated by TNF-??, IL-1??, IFN-??, NF-??B, and TLR ligands, embedding it within positive feedback loops in the tumor microenvironment.
Disruption of CCL7 in HeLa cells allows dissection of chemokine-mediated signaling relevant to cancer. HeLa cells can be induced to produce CCL7 under inflammatory stimuli, and knockout enables investigation of downstream pathways including PI3K/AKT and STAT3, which influence survival and migration. Co-culture models with immune or endothelial cells can reveal how CCL7 deficiency impairs leukocyte recruitment or angiogenesis. The polyclonal population avoids clonal artifacts while maintaining robust gene disruption, making it ideal for broad signaling studies.
This knockout cell population is suited for chemotaxis, calcium flux, and Matrigel invasion assays to evaluate migration. Western blotting for ERK1/2 phosphorylation and RT-qPCR for downstream gene expression permit detailed signal transduction analysis. ELISA of secreted CCL7 confirms protein-level knockout, and flow cytometry enables receptor expression profiling. The cells are valuable for chemokine receptor antagonist screening and for studying CCL7 in inflammation-driven cancer metastasis. For further technical information, please contact Ascent Research.
