The CD2AP Knockout MES-OV Polyclonal Cells product comprises a polyclonal population of MES-OV human ovarian adenocarcinoma cells that have been subjected to CRISPR/Cas9-mediated disruption of the CD2AP gene. This loss-of-function model is generated through targeted gene disruption using CRISPR/Cas9 technology, resulting in a heterogeneous cell pool with ablated CD2AP expression. The polyclonal format provides a robust mixture of edited alleles, enabling the study of CD2AP deficiency without the selective pressure of single-cell cloning. As a research tool, these cells are designed for investigating the scaffold protein??s role in actin dynamics, endocytosis, and tumor cell behavior.
Derived from a human ovarian adenocarcinoma, the MES-OV cell line serves as a well-characterized model of epithelial ovarian cancer, exhibiting properties relevant to tumor cell adhesion, migration, and invasion. These cells retain key epithelial characteristics and are responsive to growth factors such as EGF and TGF-beta, making them suitable for studies of receptor-mediated signaling and cytoskeletal reorganization. The MES-OV background provides a physiologically relevant context for examining CD2AP function in ovarian cancer progression, including metastasis and drug resistance.
CD2AP encodes a multifunctional scaffold protein that bridges membrane receptors, including EGFR and integrins, to the actin cytoskeleton through interactions with cortactin, CAPZ, and actin itself. Upstream activation by EGF, TGF-beta, and integrin ligands triggers CD2AP recruitment to receptor complexes, where it orchestrates endocytic trafficking by binding to Cbl, Hrs, and STAM. Downstream, CD2AP facilitates actin polymerization via cortactin, the Arp2/3 complex, and N-WASP, while also modulating signaling through PI3K/Akt and Rac1-mTOR pathways. This network positions CD2AP at the nexus of receptor internalization, focal adhesion turnover, and cell motility.
In the context of ovarian adenocarcinoma, CD2AP knockout disrupts the linkage between EGFR and the actin cytoskeleton, leading to impaired endocytosis and altered cell migration. The loss of CD2AP-mediated scaffolding compromises the assembly of cortactin-Arp2/3 complexes, reducing lamellipodia formation and invasive capacity. Additionally, crosstalk with TGF-beta signaling and focal adhesion dynamics is perturbed, potentially affecting epithelial-mesenchymal transition and drug sensitivity. This model recapitulates aspects of ovarian cancer biology where CD2AP downregulation may influence tumor aggression.
Researchers can employ this polyclonal knockout population to dissect CD2AP-dependent mechanisms in cancer cell migration and invasion using Transwell migration assays and immunofluorescence analysis of actin structures. The cells are also suited for endocytosis pathway analysis, including flow cytometry-based quantification of receptor internalization, co-immunoprecipitation of CD2AP interactors, and phospho-signaling profiling by Western blotting. Applications extend to drug resistance studies, particularly in ovarian and breast cancer models, and to signal transduction research exploring PI3K/Akt and integrin-driven pathways. For additional technical details, please contact Ascent Research to discuss your experimental requirements.
