The AIF1 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population in the DLD-1 human colorectal adenocarcinoma background with targeted disruption of the AIF1 (allograft inflammatory factor 1) gene. This gene-edited product provides a functional knockout model for investigating the role of AIF1 in actin cytoskeleton dynamics, inflammatory signaling, and cancer cell biology.
The host DLD-1 cell line is an epithelial colorectal adenocarcinoma model derived from a male patient, harboring well-characterized oncogenic mutations including KRAS G13D, and loss-of-function alterations in the tumor suppressors APC and TP53. This genetic background makes DLD-1 a widely used system for dissecting colorectal cancer progression, particularly the interplay between mutant KRAS-driven signaling, cytoskeletal reorganization, and the inflammatory tumor microenvironment. The cells maintain an adherent epithelial morphology and are suitable for a broad range of in vitro assays.
AIF1 (IBA1) is an actin-binding protein that bundles F-actin and facilitates membrane ruffling, enhancing cell motility and phagocytosis. It is induced by inflammatory stimuli such as IFN-??, TNF-??, and LPS via NF-??B and STAT1 pathways downstream of TLR4 and MyD88. Upon activation, AIF1 promotes Rac1 and Cdc42 GTPase activity, leading to actin reorganization and transcription of pro-inflammatory cytokines IL-6 and IL-1??, chemokine CCL2, and matrix metalloproteinases. AIF1 interacts directly with F-actin, calcium, and L-plastin and functions within ERK and JNK signaling modules.
In the DLD-1 colorectal cancer context, AIF1 is positioned at the intersection of cytoskeletal reorganization and tumor-promoting inflammation. KRAS G13D mutation drives constitutive activation of ERK and other effector pathways, while TP53 deficiency impairs stress responses; AIF1 may further amplify migratory and invasive properties in this background. Loss of AIF1 in this polyclonal knockout system permits detailed examination of how actin-based motility and inflammatory cytokine networks contribute to colorectal cancer cell invasion, immune cell recruitment, and metastatic potential. The model is particularly valuable for studying heterogeneity in cytoskeletal and signaling responses across the cell population.
This polyclonal knockout model is suited for migration and invasion assays (Boyden chamber), phagocytosis assays, and immunofluorescence-based cytoskeletal analysis. Inflammatory signaling can be assessed by Western blotting for phospho-NF-??B and ERK, RT-qPCR for IL-6 and CCL2, and ELISA-based cytokine quantification. NF-??B reporter assays provide additional pathway interrogation. These tools enable detailed investigation of colorectal cancer progression, tumor-associated inflammation, and cytoskeletal dynamics. For further technical details, please contact Ascent Research.
