The ITGAM Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited population derived from human ovarian carcinoma A2780 cells, featuring disruption of the ITGAM gene (CD11b). This polyclonal knockout model avoids clonal selection, providing a heterogeneous loss-of-function reagent for studying integrin alpha M functions. The product serves as a ready-to-use cellular system for investigating CD11b/CD18-mediated adhesion and signaling in epithelial cancer, bypassing the need for individual clone isolation.
A2780 is an established epithelial cell line originating from an untreated ovarian adenocarcinoma patient. It retains ovarian carcinoma characteristics, including adherent growth and epithelial markers, and is a standard model for studying tumor cell biology, drug responses, and signal transduction. The genetic manipulation of ITGAM in this background allows researchers to examine integrin alpha M contributions specifically in ovarian cancer-derived cells, separating them from stromal influences.
ITGAM encodes the alpha M integrin subunit, which pairs with CD18 (ITGB2) to form CR3 (Mac-1). This receptor binds ICAM-1, iC3b, fibrinogen, and Factor X. CR3 ligation activates Syk, then PI3K/AKT and NF-??B pathways. Upstream, ITGAM expression is regulated by PU.1, RUNX1, and cytokines like GM-CSF, TNF-??, IL-6, and TGF-??. Downstream targets include IL-1?? and TNF-??. Additional pathway components involve DAP12, PLC??, Vav, and Rac. Disruption of ITGAM interrupts adhesion-dependent signaling, providing a platform to dissect CR3 cascades.
In ovarian cancer, integrin-driven adhesion promotes peritoneal metastasis and survival. ITGAM knockout in A2780 cells enables study of CD11b??s role in cell attachment, invasion, and immune evasion. This model helps determine whether ovarian carcinoma cells rely on CR3 for resistance to anoikis and crosstalk with mesothelial layers. It also allows exploration of integrin-growth factor receptor interactions converging on AKT and NF-??B. Additionally, as ITGAM variants are linked to autoimmune and adhesion disorders, these cells can inform on epithelial contributions to inflammatory pathologies.
Researchers can employ these cells in adhesion assays with immobilized ICAM-1, migration and invasion studies, and phagocytosis experiments. Western blotting and RT-qPCR can monitor downstream activation of Syk, AKT, and NF-??B. Flow cytometry validates CD11b loss, while RNA-seq and cytokine profiling capture global expression changes. The model supports drug target validation for integrin antagonists and kinase inhibitors, and high-throughput screening for compounds with selective activity against ITGAM-deficient cells. For further information, please contact Ascent Research.
