The CD47 Knockout AGS Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population of the AGS human gastric epithelial cell line in which CD47 gene function has been disrupted. This polyclonal format provides a heterogeneous pool of knockout cells without clonal selection, allowing the study of CD47 loss in a population context that better reflects biological variability. The model is optimized for in vitro functional assays examining CD47??s roles in immune evasion, adhesion, and migration within gastric adenocarcinoma.
The AGS parental line, derived from a poorly differentiated gastric adenocarcinoma of a 54-year-old female, is a standard model for gastric cancer research. AGS cells exhibit epithelial characteristics and retain key oncogenic pathways, making them a relevant host for studying tumor cell-intrinsic mechanisms. The gastric epithelial background ensures that the phenotypic consequences of CD47 knockout are assessed in a tissue-authentic environment, thus enhancing the translational value for gastric adenocarcinoma studies.
CD47, a transmembrane protein of the immunoglobulin superfamily, functions as a ??don??t eat me?? signal through its interaction with SIRP?? on macrophages. This ligation activates tyrosine phosphatases SHP-1 and SHP-2, which dephosphorylate myosin-IIA, inhibiting phagocytic cup formation. Beyond immune regulation, CD47 contributes to cell adhesion and migration by associating with integrins ??v??3 and ??2??1 and binding thrombospondin-1 (THBS1). CD47 expression is transcriptionally controlled by HIF1A, MYC, NF-??B, and TNF, integrating hypoxia, oncogenic, and inflammatory signals. Thus, CD47 coordinates multiple pathways that jointly facilitate tumor immune escape and metastatic progression.
Disruption of CD47 in AGS gastric cancer cells is predicted to eliminate anti-phagocytic protection, rendering them susceptible to macrophage-mediated cytotoxicity, and to impair integrin-dependent adhesion and motility. This model therefore enables investigation of how CD47 loss compromises both immune evasion and invasive potential in a poorly differentiated adenocarcinoma context. It serves as a platform to explore CD47-dependent tumor-stroma interactions and to screen for synthetic vulnerabilities arising from CD47 deficiency.
This polyclonal knockout product supports a wide array of research applications. Co-culture with macrophages allows quantification of phagocytosis enhancement, while transwell migration and adhesion assays measure changes in cell motility and substrate attachment. Standard techniques such as Western blotting, flow cytometry, and RNA-seq can validate protein levels and global transcriptional responses. Furthermore, the polyclonal pool can be utilized in drug sensitivity testing, particularly for assessing CD47-targeted antibodies in combination with chemotherapeutic agents. For additional product information or technical inquiries, please contact Ascent Research.
