The AIF1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited population of A2780 cells carrying a targeted disruption of the human allograft inflammatory factor 1 (AIF1) gene. This polyclonal knockout product format consists of a heterogeneous mixture of gene-edited cells, avoiding clonal selection bottlenecks and more accurately reflecting the diversity of genetic backgrounds in tumor cell populations. The cell population is designed to serve as a loss-of-function model for AIF1, enabling robust functional studies of this key cytoskeletal and inflammatory regulator. It is suitable for use in standard cell-based assays and is provided with quality-controlled viability and growth characteristics.
The host A2780 cell line is an established model of epithelial ovarian carcinoma, originally isolated from a previously untreated patient. These cells are widely used in cancer research, particularly for investigating cisplatin sensitivity and mechanisms of drug resistance. A2780 cells exhibit characteristic ovarian cancer signaling pathways, including those governing inflammation and cytoskeletal dynamics, making them an ideal platform for studying the role of AIF1 in disease progression. The cell line’s stable and reproducible nature provides a robust background for CRISPR/Cas9-mediated gene perturbation studies.
AIF1 (Iba1) is an actin-binding protein that responds to calcium and inflammatory stimuli such as IFN-gamma, TNF-alpha, and LPS. It functions by interacting with Rac1 and the WAVE2 complex to promote actin polymerization and cell migration. Additionally, AIF1 activates NF-kB signaling, leading to transcriptional upregulation of pro-inflammatory cytokines like IL-6 and TNF-alpha. This positions AIF1 at a critical node linking immune activation to cytoskeletal reorganization. CRISPR/Cas9-mediated disruption of AIF1 expression abrogates these downstream effects, impairing cellular motility and cytokine production.
In the A2780 ovarian cancer model, AIF1 drives inflammation-mediated tumor progression and modulates cytoskeletal dynamics. Its knockout is anticipated to diminish pro-inflammatory cytokine production, including TNF-alpha and IL-6, thereby disrupting the tumor-promoting inflammatory milieu. This may alter tumor-immune cell interactions and reduce metastatic behavior. Moreover, by impairing actin remodeling, AIF1 loss could influence cellular responses to chemotherapeutic agents such as cisplatin, providing a tool to study the intersection of inflammation, cytoskeletal regulation, and drug resistance in ovarian cancer.
This AIF1 knockout polyclonal cell population is ideal for assays including Western blotting and RT-qPCR to confirm gene disruption and quantify inflammatory cytokines such as IL-6 and TNF-alpha. Immunofluorescence can visualize actin and AIF1 localization, while Transwell migration and invasion assays evaluate motility changes. NF-kB reporter systems and flow cytometric analysis of immune markers provide insights into signaling and phenotype. Cisplatin sensitivity tests permit direct assessment of drug resistance. Together, these approaches enable detailed mechanistic studies of AIF1 in ovarian cancer biology. For additional inquiries, please contact Ascent Research.
