The CCL7 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HT29 human colorectal adenocarcinoma cell line. This product enables loss-of-function studies of CCL7, a CC chemokine that regulates leukocyte recruitment and inflammation. The polyclonal pool contains a heterogeneous mix of edited alleles, providing a robust model for investigating CCL7-dependent signaling without single-cell clonal selection. Researchers can employ this knockout model to interrogate chemokine networks in a genetically perturbed background that retains the epithelial characteristics of the parental HT29 line.
HT29 cells are a well-characterized human colorectal adenocarcinoma cell line isolated from a primary tumor. This line serves as a foundational model for colorectal cancer biology and intestinal epithelial physiology. HT29 cells exhibit robust growth in culture, are amenable to genetic manipulation, and retain key features of intestinal epithelium, including polarization and mucin production. These properties make HT29 cells particularly suitable for studying the interplay between epithelial cells and the immune microenvironment in colorectal cancer and inflammatory conditions.
CCL7 functions as a potent chemoattractant for monocytes, eosinophils, basophils, and T cells by signaling through multiple chemokine receptors including CCR1, CCR2, CCR3, and CCR5. Its expression is transcriptionally regulated by pro-inflammatory stimuli such as TNF-alpha, IL-1 beta, and IFN-gamma via NF-kappa B and AP-1. Downstream, receptor engagement activates PI3K, Akt, ERK, and p38 MAPK pathways, ultimately promoting cell migration and inflammatory responses. CCL7 also interacts with glycosaminoglycans and other CC chemokines like CCL2 and CCL8, forming a complex signaling network that modulates leukocyte trafficking and tissue homeostasis.
In HT29 cells, CCL7 knockout likely disrupts autocrine and paracrine loops that influence tumor progression and immune cell recruitment. The loss of CCL7-mediated signaling may alter the expression of downstream effectors such as NF-kappa B, IL-6, MMPs, and VEGF, which are critical in colorectal cancer invasion and angiogenesis. This model thus provides a valuable platform to dissect the role of chemokine-driven inflammation in epithelial barrier dysfunction, tumor-stroma interactions, and the metastatic niche within the colorectal cancer microenvironment.
Typical research applications include cancer immunology, chemokine signaling dissection, and tumor microenvironment studies. The knockout cells are compatible with chemotaxis assays, ELISA-based cytokine profiling, Western blotting, RT-qPCR, and RNA-seq. They can be used for drug screening targeting chemokine receptors, co-culture systems to study immune-epithelial crosstalk, and migration/invasion assays. For technical inquiries, please contact Ascent Research.
