The CD47 Knockout MES-OV Polyclonal Cells comprise a CRISPR/Cas9-mediated gene-disrupted polyclonal knockout cell population targeting the CD47 gene in the MES-OV human ovarian cancer cell line. This product is supplied as a heterogeneous pool of cells harboring diverse loss-of-function mutations, generated by transient Cas9 and guide RNA delivery without single-cell cloning, thereby preserving the intrinsic variability of a polyclonal knockout model. The resulting population exhibits reduced CD47 protein expression, offering a versatile tool for studying CD47-dependent phenotypes in an epithelial ovarian cancer context without the constraints of monoclonal selection.
Derived from a patient with ovarian endometrioid carcinoma, the MES-OV cell line represents an adherent epithelial cell model widely employed in ovarian cancer research. MES-OV cells retain key features of the primary tumor, including oncogenic signaling networks relevant to tumorigenesis and drug response. Their use as a host for CRISPR/Cas9 editing allows direct interrogation of gene function in a disease-relevant background, facilitating translational studies in ovarian carcinoma biology.
CD47 functions as a critical anti-phagocytic signal by engaging the inhibitory receptor SIRP?? on macrophages, leading to recruitment and phosphorylation of SHP-1 and SHP-2 phosphatases, which in turn suppress myosin-II-mediated cytoskeletal rearrangements required for phagocytosis. Upstream, CD47 expression is transcriptionally activated by TNF-??, IFN-??, and HIF-1?? through NF-??B signaling, linking inflammatory and hypoxic tumor microenvironments to immune evasion. Beyond immune regulation, CD47 interacts with thrombospondin-1 and integrin ??v??3 and ??2??1 heterodimers, modulating focal adhesion kinase (FAK)-PI3K-Akt signaling to influence cell adhesion and migration. This multifaceted signaling network establishes CD47 as a node connecting immune checkpoint function with integrin-driven motility.
In the context of MES-OV ovarian endometrioid carcinoma cells, CD47-mediated anti-phagocytic signaling is hypothesized to promote tumor immune escape, a process commonly associated with disease progression. Loss of CD47 in this model disrupts the CD47-SIRP?? axis, potentially enhancing macrophage-mediated clearance and altering integrin-dependent adhesive properties. This knockout model enables systematic dissection of CD47’s role in ovarian cancer cell-macrophage crosstalk and its contribution to the malignant phenotype, providing a physiologically relevant system for evaluating therapeutic interventions.
Researchers can employ these polyclonal knockout cells in co-culture phagocytosis assays to measure macrophage engulfment, flow cytometry to confirm CD47 ablation, and western blotting to assess downstream SHP-1/SHP-2 phosphorylation or FAK-Akt activation. Immunofluorescence and migration assays further elucidate CD47’s impact on cytoskeletal organization and motility, while antibody blocking experiments validate anti-CD47 therapeutic candidates. These applications support investigations into ovarian cancer immune evasion, macrophage checkpoint blockade, and tumor microenvironment dynamics. For additional information or technical support, please contact Ascent Research.
