The AIF1 Knockout 786-O Polyclonal Cells provide a genetically disrupted population of the 786-O renal carcinoma cell line, engineered via CRISPR/Cas9-mediated targeted disruption of the Allograft Inflammatory Factor 1 (AIF1) gene. This polyclonal knockout product is supplied as a mixed population of edited cells, enabling loss-of-function studies without the selection of a single clonal isolate. The product is designed for researchers investigating the roles of AIF1 in inflammatory signaling, cytoskeletal dynamics, and cancer progression, and is a versatile tool for generating reproducible knockout phenotypes in a well-characterized renal cancer model.
The host cell line, 786-O, is a human clear cell renal cell adenocarcinoma epithelial line that harbors a well-documented VHL mutation, leading to constitutive activation of hypoxia-inducible factor pathways. Originating from a primary tumor, 786-O cells are widely used in renal carcinoma research to study tumorigenesis, drug response, and the tumor microenvironment. Their genetic background makes them particularly suitable for examining the intersection of oncogenic signaling and inflammation, providing a relevant context for probing the functional contributions of AIF1.
AIF1, also known as Iba-1, is a calcium-binding protein that bundles actin filaments and participates in immune cell activation and migration. In myeloid cells, it is transcriptionally induced by interferon-gamma (IFN-??), tumor necrosis factor-alpha (TNF-??), interleukin-1beta (IL-1??), and lipopolysaccharide (LPS) through Toll-like receptor (TLR) agonists, linking inflammatory stimuli to cytoskeletal reorganization. AIF1 interacts directly with actin and calmodulin in a calcium-dependent manner, and its downstream effects include promoting actin polymerization, cell motility, and the production of pro-inflammatory cytokines such as IL-6 and TNF-??. These functions place AIF1 at the convergence of NF-??B signaling (involving NFKB1 and RELA), MAPK cascades (via MAPK1), and RhoA-mediated actin remodeling pathways.
In the 786-O renal carcinoma model, AIF1 knockout is expected to disrupt calcium-dependent actin bundling and attenuate cytokine- and TLR-driven signaling, potentially diminishing cell migration and altering the secretome. Given that AIF1 is implicated in chronic inflammation and tumor-associated macrophage activation, its loss in carcinoma cells may impact interactions with immune components of the tumor microenvironment. This model thus serves as a platform to dissect tumor-intrinsic inflammatory responses and their contribution to clear cell renal cell carcinoma progression.
Applications for these polyclonal AIF1 knockout cells span a range of cancer biology and immunological studies. Researchers can employ them in transwell migration and invasion assays to assess motility changes, immunofluorescence staining of F-actin to visualize cytoskeletal alterations, and RT-qPCR or ELISA profiling of cytokine expression (e.g., IL-6, TNF-??) upon stimulation. Co-culture experiments with immune cells, coupled with flow cytometric adhesion assays, enable investigation of tumor-immune interactions. Western blotting for AIF1 confirms knockout efficiency across the population. For further details on this cell product, please contact Ascent Research.
