The CCL7 Knockout PaTu 8988t Polyclonal Cells provide a polyclonal population of the PaTu 8988t pancreatic ductal adenocarcinoma cell line engineered by CRISPR/Cas9 to disrupt the CCL7 gene, resulting in a loss-of-function model for the chemokine CCL7. This polyclonal format captures heterogeneous edit outcomes, avoiding clonal artifacts, and is suitable for functional analyses of chemokine signaling in cancer biology.
The host cell line PaTu 8988t originates from a liver metastasis of human PDAC and carries oncogenic KRAS G12D and TP53 mutations, which are central drivers of pancreatic tumorigenesis, immune evasion, and metastatic propensity. This background makes it an ideal platform to examine how CCL7-mediated inflammation intersects with established oncogenic pathways.
CCL7 is a CC-chemokine that signals through the receptors CCR1, CCR2, and CCR3 to chemoattract monocytes, eosinophils, and T cells. Its transcription is activated by TNF-alpha, IL-1beta, IFN-gamma, and LPS via NF-kB, STAT1, and AP-1. Ligand-receptor engagement triggers phosphorylation of JAK2 and STAT3, as well as MAPK1 and MAPK3, leading to upregulation of matrix metalloproteinase MMP9 and adhesion molecule ICAM1. CCL7 also interacts with glycosaminoglycans and CXCL8, integrating into broader chemokine networks.
In the PaTu 8988t context, CCL7 knockout eliminates the ligand for CCR1/2/3, disrupting downstream JAK/STAT and MAPK signaling cascades that drive pro-inflammatory gene expression and macrophage recruitment. This loss is predicted to impair tumor-associated inflammation and metastatic niche formation, offering a controlled system to dissect chemokine-dependent tumor-stroma interactions in pancreatic cancer.
Researchers can apply this model to investigate CCL7’s function in the immune microenvironment, macrophage polarization, and T cell trafficking. Representative assays include Western blot for CCL7 and phospho-STAT3, ELISA for secreted CCL7, chemotaxis assays, co-culture with immune cells, RNA-seq, and xenograft tumor growth studies. These cells also enable screening for inhibitors targeting CCL7 signaling. For more information or to request validation data, please contact Ascent Research.
