The CD46 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt CD46 gene expression in the MES-OV human ovarian clear cell carcinoma cell line. This loss-of-function model provides a defined genetic background for investigating the roles of CD46 in complement regulation, pathogen recognition, and intracellular signaling. The polyclonal format preserves typical heterogeneity of pooled editing, enabling robust experimental replication without clonal biases. These cells serve as a reliable platform for dissecting CD46-dependent phenotypes in a disease-relevant context.
The parental MES-OV cell line is derived from human ovarian clear cell carcinoma and exhibits adherent epithelial morphology. As an established model for ovarian cancer studies, MES-OV retains key oncogenic features, including aberrant growth signaling and invasive potential. Introducing CD46 knockout into this background creates a clinically relevant system for studying complement-mediated tumor surveillance, immune evasion mechanisms, and the interplay between complement regulators and cancer progression. The adherent phenotype facilitates standardized culture, transfection, and high-content imaging workflows.
CD46 is a membrane-bound complement regulatory protein that functions as a cofactor for the serine protease factor I, enabling specific cleavage of C3b and C4b. This activity prevents the formation of C3/C5 convertases and subsequent assembly of the membrane attack complex, thereby protecting host cells from autologous complement attack. CD46 also serves as a cellular receptor for measles virus and other pathogens, binding the measles virus hemagglutinin. Its expression is transcriptionally upregulated by inflammatory stimuli including IL-1?? and TNF-?? through NF-??B activation. Downstream, CD46 modulates IL-10 secretion, promotes regulatory T cell induction, and influences Notch-dependent T cell differentiation, highlighting its multifaceted roles in innate and adaptive immunity.
In the MES-OV ovarian cancer context, CD46 knockout abrogates complement resistance, rendering cells susceptible to complement-dependent cytotoxicity and enhanced C3b opsonization. This deficiency recapitulates tumor cell vulnerability observed during antibody-based immunotherapies and facilitates study of complement evasion strategies in cancer. Moreover, loss of CD46-mediated signaling may alter the tumor microenvironment by disrupting IL-10-driven immunosuppression and T cell differentiation pathways. Thus, these polyclonal knockout cells provide a powerful tool to disentangle the complement-dependent and -independent contributions of CD46 to ovarian cancer pathogenesis.
Typical applications include complement-dependent cytotoxicity assays, flow cytometric analysis of C3b surface deposition, western blotting for complement pathway components, RT-qPCR for target gene expression, and immunofluorescence imaging of immune complex formation. These cells are also suited for RNA-seq transcriptomic profiling and viability assays under complement-rich conditions. Researchers can leverage this model to investigate CD46’s role in cancer immune evasion, infectious disease receptor biology, and immunomodulatory signaling. For further information on lot-specific performance and customization, please contact Ascent Research.
