The CCL7 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 143B osteosarcoma cell line. This loss-of-function tool provides a heterogeneous pool of cells with targeted disruptions in the CCL7 gene, circumventing the biases of clonal selection. It is designed for functional studies of CCL7 in cancer biology and immune cell recruitment.
The parental 143B cell line is a widely used osteosarcoma model originating from the TE85 lineage. It harbors a p53 tumor suppressor mutation and exhibits a highly metastatic phenotype, commonly metastasizing to the lungs. These features make it an ideal system for studying bone cancer progression and metastasis, as well as for evaluating the contribution of specific genes to tumor aggressiveness and microenvironmental interactions.
CCL7 encodes a chemokine that acts as a chemoattractant for monocytes and T cells through binding to the G-protein coupled receptors CCR1, CCR2, and CCR3. Receptor engagement initiates signaling via JAK2/STAT3, MAPK1/ERK, and PI3K/AKT cascades, ultimately modulating NF-??B transcriptional activity and integrin-mediated adhesion. CCL7 expression is induced by TNF-?? and IL-1?? through NF-??B and AP-1 transcription factors. Downstream, CCL7 promotes STAT3 phosphorylation, ERK activation, and AKT signaling, which collectively drive cell migration and pro-inflammatory gene expression. Interactions with the atypical chemokine receptor DARC and heparan sulfate proteoglycans influence chemokine localization and activity within the tumor microenvironment.
In the 143B osteosarcoma context, CCL7 knockout is expected to disrupt chemotactic signals that recruit monocytes and T cells, thereby altering the immune landscape and potentially impairing metastatic spread. This model enables investigation of how tumor-intrinsic CCL7 contributes to osteosarcoma progression, immune evasion, and the formation of pre-metastatic niches in organs such as the lungs. It also provides a platform to study the interplay between chemokine signaling and the p53-mutated background in governing metastatic behavior.
Researchers can apply these cells in co-culture assays with immune cells to measure monocyte and T cell migration, in Transwell invasion studies to assess metastatic capacity, and in phospho-kinase arrays to profile signaling changes. The model is compatible with RNA-seq and RT-qPCR for transcriptomic analyses, and with ELISA or flow cytometry for protein-level studies. It supports drug target validation in chemokine-related diseases including asthma, atherosclerosis, and rheumatoid arthritis, and aids in testing CCR antagonists. For technical inquiries, please contact Ascent Research.
