The AIF1 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 769-P renal clear cell carcinoma epithelial cell line. This product provides a genetically heterogeneous pool of edited cells with disruption of the AIF1 gene, enabling loss-of-function studies in a biologically relevant renal cancer background. The polyclonal format avoids clone-specific artifacts and offers a robust model for investigating AIF1-dependent phenotypes.
The parental 769-P cell line, isolated from a human clear cell renal cell carcinoma, is widely used as a model for renal cell carcinoma (RCC). As an adherent epithelial line, 769-P retains key molecular features of RCC, including aberrant signaling pathways and tumorigenic properties, making it suitable for examining cytoskeletal dynamics, cell migration, and epithelial-associated inflammatory responses.
AIF1 encodes a calcium-binding protein that organizes the actin cytoskeleton, regulates membrane ruffling, and drives pro-inflammatory signaling. Upregulated by IFNG, TNF, IL1B, and LPS, AIF1 function is calcium-dependent and involves interactions with F-actin, LCP1, and RAC1. It promotes actin crosslinking and ARP2/3-mediated filament branching, leading to enhanced cell migration and phagocytosis. Downstream, AIF1 activates NF-??B and MAPK1 pathways, inducing expression of cytokines IL6, CCL2, TNF, and matrix metalloproteinase MMP9. Thus, AIF1 knockout disrupts actin remodeling and attenuates inflammatory cytokine production.
In the 769-P renal carcinoma background, AIF1 knockout allows dissection of its role in RCC-associated processes such as actin-driven invasion and inflammatory signaling. Renal clear cell carcinomas often exhibit activated inflammatory pathways; thus, AIF1-depleted 769-P polyclonal populations help assess impacts on migration, adhesion, and cytokine secretion. Although AIF1 is classically studied in macrophages, this model also serves as a tool for investigating epithelial-immune cross-talk within the tumor microenvironment.
Researchers can employ these cells in wound healing and transwell migration assays to quantify AIF1-dependent motility. Phagocytosis assays, F-actin staining, and RT-qPCR/Western blotting of targets such as IL6, CCL2, MMP9, and RAC1/NF-??B components enable comprehensive phenotyping. Applications include drug screening for anti-migratory agents in RCC, inflammation mechanism studies, and tumor microenvironment research. For further technical information and ordering details, please contact Ascent Research.
