The CD46 Knockout HGC-27 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD46 gene has been disrupted in the HGC-27 human gastric carcinoma cell line. This heterogeneous knockout pool is generated through CRISPR/Cas9-mediated target-gene disruption, enabling loss-of-function analysis without the constraints of clonal selection. The model is designed for researchers investigating CD46-dependent mechanisms in complement regulation, immune modulation, and pathogen recognition, and it supports a wide range of functional assays.
The HGC-27 host cell line is an epithelial cell model derived from the metastatic lymph node of a patient with undifferentiated gastric adenocarcinoma. It is widely employed in gastric cancer research due to its retention of key features of aggressive disease, including invasive potential and relevant signaling pathway activity. HGC-27 cells provide a physiologically relevant background for dissecting molecular drivers of tumor progression, metastasis, and immune evasion in the gastric microenvironment.
CD46 encodes a type I transmembrane glycoprotein that acts as a membrane cofactor protein (MCP) for the serine protease factor I, promoting the proteolytic inactivation of complement components C3b and C4b to protect host cells from autologous lysis. In concert with other regulators such as CD55 and CD59, CD46 maintains complement homeostasis. Beyond complement control, CD46 serves as a receptor for measles virus hemagglutinin and bacterial adhesins, and it engages in immune modulation through T-cell differentiation and IL-10 production. CD46 expression is transcriptionally upregulated by TNF-??, IL-1??, IFN-??, SP1, and NF-??B. Upon ligand binding, CD46 activates downstream PI3K/AKT and MAPK/ERK signaling cascades, interacts with tetraspanins CD9 and CD151, and associates with PD-L1, collectively influencing cell survival, autophagy, and immune escape.
In gastric cancer, CD46 is frequently overexpressed and contributes to tumor immune evasion by limiting complement deposition and by transducing signals that promote proliferation, migration, and invasion. The CD46 knockout HGC-27 model allows researchers to dissect CD46-specific contributions to complement resistance and intracellular signaling in a gastric cancer context. By ablating CD46 function, this polyclonal population facilitates the analysis of complement-dependent cytotoxicity and the mapping of CD46-dependent signaling nodes critical for gastric cancer progression, offering a powerful tool for studying tumor?Cimmune interactions.
This knockout cell product is suited for applications including the systematic investigation of complement evasion mechanisms, the evaluation of measles virus entry pathways, and the development of targeted therapeutics for CD46-overexpressing malignancies. Representative assays compatible with the model include flow cytometry for CD46 surface expression validation, complement-mediated cytotoxicity assays, western blotting for C3b cleavage and phospho-AKT/ERK profiling, viral infection assays, cell migration and invasion assays, and drug sensitivity screening. The polyclonal nature reduces clonal bias, providing a robust platform for functional genomics and drug discovery studies in gastric cancer. Further technical details can be obtained from Ascent Research.
