The CD55 Knockout 786-O Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CD55 gene. This product provides a heterogeneous pool of cells with targeted disruption of CD55, enabling investigation of its roles without single-cell clonal selection. The gene-edited population is suited for researchers requiring a physiologically relevant knockout model that maintains the diverse cellular behaviors inherent to polyclonal cultures.
The host cell line, 786-O, is a human renal cell adenocarcinoma line widely employed as a model for clear cell renal cell carcinoma (ccRCC). Derived from a primary tumor, 786-O cells harbor characteristic genetic alterations, including VHL deficiency, which stabilizes hypoxia-inducible factor 1-alpha (HIF-1alpha) and drives constitutive expression of vascular endothelial growth factor (VEGF) and other hypoxia-responsive genes. These features recapitulate key aspects of ccRCC biology, making 786-O an ideal platform for studying tumor-specific signaling, immune evasion, and therapy resistance.
CD55, also known as decay-accelerating factor (DAF), is a glycosylphosphatidylinositol (GPI)-anchored membrane protein that functions as a critical complement regulator. By binding to C3b and C4b, CD55 accelerates the decay of C3 and C5 convertases, thereby protecting cells from complement-mediated lysis. Beyond complement inhibition, CD55 participates in non-canonical signaling pathways through its association with lipid raft microdomains and Src family kinases. It can be transcriptionally upregulated by pro-inflammatory cytokines such as TNF-alpha and IL-1beta, bacterial lipopolysaccharide (LPS), and the HIF-1alpha/VEGF axis. Downstream consequences of CD55 disruption include enhanced C3b deposition, increased complement susceptibility, altered T cell proliferation, and modulation of MAPK/ERK signaling. Additionally, CD55 interacts with the adhesion G protein-coupled receptor CD97, further linking complement regulation to cell adhesion and migration.
In the 786-O ccRCC context, CD55 knockout provides a powerful tool to dissect the interplay between complement resistance and tumor immune evasion. Renal carcinomas often exploit CD55 to avoid complement-dependent cytotoxicity, contributing to therapeutic resistance. Removal of this protective mechanism by gene disruption sensitizes 786-O cells to complement attack, enabling studies of antibody-based therapies and the tumor microenvironment. Moreover, the knockout facilitates examination of CD55-mediated signal transduction through Src, Akt, and ERK, which may influence proliferation, migration, and drug response. The polyclonal nature of the product captures a range of knockout efficiencies, reflecting the heterogeneity of tumor cell populations.
This product is suitable for a variety of research applications, including complement-dependent cytotoxicity assays to evaluate therapeutic antibodies, flow cytometry-based quantification of C3b deposition, and Western blot analysis confirming CD55 deficiency. Functional studies can assess cell proliferation, migration, and invasive behavior, while phospho-specific analyses probe Akt and ERK activation. Researchers investigating the regulation of the actin cytoskeleton or the PI3K-Akt pathway will find this model valuable for exploring CD55??s involvement in these networks. For additional technical details, please contact Ascent Research.
