The CD55 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HGC-27 human gastric carcinoma cell line. This product provides a loss-of-function model for CD55 (decay-accelerating factor, DAF), a critical negative regulator of complement activation. The polyclonal knockout cell population is derived through CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous mix of edited alleles that ablate CD55 protein expression. This approach supports robust phenotypic screening and functional studies without the biases inherent to single-clone selection.
The HGC-27 cell line is an adherent, epithelial-like human gastric carcinoma line originally established from a lymph node metastasis of a gastric adenocarcinoma. This cell line is widely utilized as a model system for studying gastric cancer biology, including tumor progression, metastasis, and therapeutic resistance. Its epithelial origin and malignant properties make it particularly relevant for investigating how complement regulatory proteins contribute to immune evasion within the tumor microenvironment. The HGC-27 background offers a clinically pertinent platform for exploring CD55 function in a context that closely mirrors advanced gastric cancer.
CD55 is a glycosylphosphatidylinositol (GPI)-anchored membrane protein that functions as a key negative regulator of the complement cascade. Mechanistically, CD55 binds to C3b and C4b, accelerating the dissociation of classical and alternative pathway C3 and C5 convertases, thus preventing the formation of the membrane attack complex and reducing anaphylatoxin generation. Its expression is transcriptionally regulated by TNF-alpha, IL-1beta, and LPS via NF-kappaB pathways. CD55 also interacts with CD97 and acts as a cellular receptor for echovirus and coxsackievirus B. It cooperates with CD59 and CR1 to finely modulate innate immune responses.
In HGC-27 cells, CD55 overexpression confers resistance to complement-dependent cytotoxicity, an immune evasion tactic exploited by gastric carcinomas. Knockout of CD55 restores complement sensitivity, rendering cells vulnerable to lysis and opsonization. This enables dissection of immune escape mechanisms and assessment of complement-activating therapeutics. Additionally, CD55’s involvement in paroxysmal nocturnal hemoglobinuria and autoimmunity extends the model’s applicability.
The CD55 Knockout HGC-27 Polyclonal Cells support diverse assays: flow cytometry for CD55 expression, complement-dependent cytotoxicity (CDC) assays, western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation with C3b or CD97, and viral infection models. Applications encompass complement biology, immune evasion studies, and the development of complement-targeted cancer therapies. For inquiries, contact Ascent Research.
