The CD55 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma epithelial cell line. This product features targeted disruption of the CD55 gene, leading to loss of CD55 protein expression across a heterogeneous pool of edited cells. As a polyclonal knockout model, it provides a versatile tool for studying complement regulation and immune evasion in cancer without the limitation of single-clone selection. The knockout population is suitable for a wide range of functional assays and can be used to interrogate both canonical and non-canonical roles of CD55 in tumor biology.
The parental A2780 cell line was established from an untreated patient with ovarian adenocarcinoma and serves as a well-characterized model for human ovarian carcinoma. These epithelial cells retain key characteristics of the original tumor, including growth properties and signaling networks relevant to ovarian cancer progression. A2780 cells are widely used in drug discovery, cancer biology, and immunology to investigate mechanisms of chemoresistance, metastasis, and immune surveillance. The availability of a CD55 knockout in this background enables precise dissection of complement-mediated tumor cell clearance and associated signaling pathways.
CD55, also known as decay-accelerating factor (DAF), is a glycosylphosphatidylinositol (GPI)-anchored membrane protein that inhibits the complement cascade by accelerating the decay of C3 and C5 convertases, thus preventing membrane attack complex (MAC; C5b-9) formation and complement-dependent lysis. CD55 expression is upregulated by pro-inflammatory stimuli such as TNF-?? and IL-1?? through NF-??B and CREB transcription factors. The protein directly interacts with complement fragments C3b and C4b, as well as the adhesion G protein-coupled receptor CD97, and its activity modulates downstream complement activation and T-cell costimulatory signals.
In the context of A2780 ovarian carcinoma cells, CD55 contributes to immune evasion by inhibiting complement-mediated cytotoxicity, a mechanism often exploited by tumors to escape innate immune attack. CRISPR-mediated gene disruption removes this protective barrier, rendering cells more susceptible to complement-dependent lysis and potentially enhancing antitumor immune responses. This model provides a powerful system for exploring how loss of CD55 affects tumor cell viability under complement challenge, as well as for evaluating the contribution of complement regulatory proteins to ovarian cancer pathogenesis and therapy resistance.
Typical applications include complement-dependent cytotoxicity (CDC) assays, screening therapeutic antibodies for CDC augmentation, and evaluating complement-targeted drugs. Knockout validation can be performed by flow cytometry and Western blotting, and downstream functional studies via apoptosis assays, RNA sequencing, and MTT viability assays are readily conducted. These polyclonal knockout cells provide a physiologically relevant platform for drug discovery and mechanistic research. For technical specifications and ordering details, please contact Ascent Research.
