The AIF1 Knockout Ca Ski Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population targeting the AIF1 gene in the Ca Ski cervical carcinoma cell line. This heterogeneous pool enables loss-of-function studies without requiring a clonal isolate, suitable for pooled functional assays and screens in an HPV-16-positive epithelial context.
The Ca Ski cell line, derived from a human cervical squamous cell carcinoma, harbors integrated HPV-16 genomes and expresses viral oncoproteins E6 and E7, which inactivate p53 and Rb pathways. This well-characterized epithelial model is routinely used to investigate tumor invasion, metastasis, and the inflammatory tumor microenvironment, providing a relevant background for AIF1 research.
AIF1 encodes the actin-binding protein Iba1, which regulates cytoskeletal rearrangements and inflammatory signaling. It interacts with ??-actin (ACTB), F-actin, L-plastin, and ITGAM in a Ca2?-dependent manner. Upon stimulation by IFN-??, TNF-??, or LPS through TLR4, AIF1 activates NF-??B via MyD88 and I??B??, driving transcription of IL-6, IL-1??, and CCL2. AIF1 also coordinates RAC1 and CDC42 to activate PAK1 and LIMK1, leading to cofilin-mediated actin remodeling essential for migration and phagocytosis.
In the Ca Ski background, AIF1 knockout permits dissection of its role in HPV-positive cervical cancer. AIF1 upregulation is linked to enhanced invasion and NF-??B-dependent expression of MMP9 and CCL2, which remodel the extracellular matrix and recruit immune cells. This model allows interrogation of crosstalk between AIF1-driven inflammation and HPV oncogene signaling, and can be applied to study atherosclerosis and rheumatoid arthritis where AIF1-mediated inflammatory activation is central.
Researchers can employ Transwell invasion assays, phalloidin staining, Western blotting, and immunofluorescence to assess migration and actin dynamics. ELISA and flow cytometry quantify cytokines like IL-6, while RNA-seq reveals transcriptomic effects. Co-immunoprecipitation examines disrupted interactions with ??-actin or ITGAM. Key applications include investigating AIF1-dependent migration in cervical cancer, analyzing inflammatory signaling, studying actin dynamics, and evaluating AIF1 as a therapeutic target. For further details, contact Ascent Research.
