The CD55 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the MES-OV human ovarian endometrioid carcinoma cell line, with targeted disruption of the CD55 gene. This loss-of-function model eliminates CD55-mediated complement inhibition, sensitizing cells to complement-dependent cytotoxicity and enabling detailed investigation of tumor immune evasion mechanisms.
MES-OV is an adherent epithelial cell line isolated from a human ovarian endometrioid adenocarcinoma, widely used as a robust model for ovarian cancer research. The cells retain oncogenic drivers and permit genetic manipulation, making them ideal for studying cancer cell-intrinsic resistance to complement attack. Their ovarian carcinoma origin provides a clinically pertinent system to evaluate therapies that restore immune-mediated tumor killing.
CD55 (decay-accelerating factor) is a GPI-anchored protein that protects host cells from complement by accelerating decay of C3 and C5 convertases. It binds C3b and C4b and interacts with factor B and factor D to block convertase amplification, thereby preventing membrane attack complex formation and cell lysis. CD55 expression is upregulated by TNF-alpha, IL-1, complement activation products, and inflammatory stimuli, linking inflammatory signaling to cytoprotection. The protein also interacts with CD97, integrating complement regulation with leukocyte adhesion. Knockout of CD55 ablates these functions, exposing cells to opsonization and MAC-mediated damage.
In the MES-OV ovarian cancer context, CD55 overexpression often enables immune escape by shielding tumor cells from complement. Disruption of CD55 removes this protection, allowing researchers to systematically analyze complement-dependent cytotoxicity in carcinoma cells. The polyclonal knockout format introduces heterogeneous edits, better modeling the diversity of tumor cell populations and pooled CRISPR screens, and facilitating studies of phenotypic variability in complement sensitivity.
This product supports applications including complement-mediated killing assays (cell viability and LDH release), flow cytometry to confirm CD55 ablation, western blotting, immunofluorescence, and RT-qPCR. It is well-suited for drug screens targeting complement components such as factor B or C5, for modeling paroxysmal nocturnal hemoglobinuria and autoimmune hemolytic anemias, and for evaluating novel complement inhibitors. For technical support, contact Ascent Research.
