The CD63 Knockout 143B Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line, enabling loss-of-function studies of the tetraspanin CD63. This polyclonal pool consists of a genetically heterogeneous collection of cells carrying diverse disruptive edits in the CD63 gene, avoiding the clonal artifacts associated with single-cell-derived lines and offering a robust model for evaluating CD63-dependent phenotypes across a broad cellular context.
The 143B cell line is a widely used human osteosarcoma model originating from a bone cancer patient, characterized by a homozygous TP53 mutation and a highly metastatic phenotype. These cells exhibit aggressive migratory and invasive properties, making them a standard platform for investigating mechanisms of tumor metastasis, cell adhesion, and bone cancer biology. The TP53 deficiency recapitulates a common genetic lesion in aggressive cancers, providing a clinically relevant background for studying gene function in advanced disease settings.
CD63 is a member of the tetraspanin superfamily that organizes membrane microdomains, where it physically interacts with other tetraspanins such as CD9 and CD81 to form the core of the tetraspanin web. Through these interactions, CD63 regulates exosome biogenesis and cargo sorting, integrin trafficking, and cell adhesion. The protein interacts with integrins, SNAP-23, and E-cadherin to orchestrate downstream signaling cascades, including MAPK/ERK and Rac1 pathways, thereby modulating cell migration and metastatic behavior. Upstream, CD63 expression and activity are influenced by cellular stress, cytokines, and growth factors, linking extracellular cues to membrane dynamics and signal transduction.
In the TP53-mutant, highly metastatic 143B background, disruption of CD63 provides a powerful tool for dissecting its contributions to exosome-mediated intercellular communication, integrin-dependent adhesion, and invasive capacity. This polyclonal knockout model allows researchers to study how loss of CD63 alters the formation and function of the CD63-CD9-CD81 complex and the subsequent effects on ??-catenin, ERK1/2, and Rac1 signaling. The model is particularly relevant for exploring mechanisms that drive osteosarcoma dissemination and for identifying vulnerabilities in tetraspanin-regulated pathways that could be exploited for therapeutic intervention.
These polyclonal knockout cells are ideally suited for applications including exosome biology, tumor metastasis, cell adhesion, and immune modulation studies. Representative assays include exosome isolation and characterization, western blotting, immunofluorescence, adhesion assays, migration/invasion assays, and flow cytometry. The model further supports drug delivery research and investigations into viral infection mechanisms where CD63 plays a role. For further information, customization options, or technical support, please contact Ascent Research.
