The CD2AP Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for studying CD2AP function in biomedical research. This product comprises a heterogeneous pool of A2780 cells with targeted disruption of the CD2AP gene, generated using CRISPR/Cas9-mediated gene editing. As a polyclonal knockout, it provides a versatile loss-of-function model without clonal isolation, reflecting a population-level knockout effect. The gene-edited cells enable investigation of CD2AP-dependent processes in an epithelial ovarian cancer background.
The parental A2780 cell line is a well-characterized human ovarian carcinoma epithelial cell line derived from an untreated patient. It serves as a widely used model for ovarian cancer research, particularly for studying tumor cell signaling, adhesion, migration, and drug response. The A2780 line exhibits epithelial morphology and harbors genetic alterations relevant to ovarian carcinogenesis. Its ability to form tumors in immunocompromised mice makes it suitable for in vitro and in vivo metastasis assays. This host background provides a clinically relevant context for examining the role of CD2AP in ovarian cancer progression.
CD2AP (CD2-associated protein) encodes an adaptor molecule that couples membrane receptors to the actin cytoskeleton, orchestrating endocytosis, cell adhesion, and migration. CD2AP interacts with CD2, nephrin, podocin, and integrins, and directly binds actin, CAPZ, cortactin, and CIN85. It forms part of a signaling network that includes the TCR/CD3 complex, nephrin signaling, and PI3K-AKT pathways. Upon receptor engagement, CD2AP facilitates recruitment of downstream effectors such as Rac1, Vav1, and the Arp2/3 complex via WAVE, promoting actin polymerization. CD2AP also modulates endocytic trafficking through interactions with Rab4 and CIN85, and participates in focal adhesion dynamics by linking integrin engagement to AKT and ERK activation. Knockout of CD2AP disrupts these molecular connections, impairing actin cytoskeleton reorganization and signal transduction.
In the A2780 ovarian carcinoma context, CD2AP knockout provides a powerful tool to dissect its contributions to tumor cell motility and invasion. Loss of CD2AP attenuates integrin-mediated signaling and focal adhesion turnover, leading to reduced cell migration and extracellular matrix invasion??critical steps in ovarian cancer metastasis. Moreover, CD2AP??s established roles in podocyte slit diaphragm assembly link this model to podocyte-related mechanisms, enabling cross-tissue studies of nephrin signaling in non-kidney cells. This knockout model thus bridges cancer cell biology and podocyte pathobiology, offering insights into shared adaptor protein functions.
Researchers can employ this polyclonal knockout cell population in diverse experimental workflows. Typical applications include Western blotting to confirm CD2AP protein absence, co-immunoprecipitation for protein interaction mapping, immunofluorescence staining of F-actin to assess cytoskeletal changes, and wound healing or transwell assays to quantify migration and invasion defects. The model supports drug target validation for focal segmental glomerulosclerosis (FSGS) and ovarian cancer, as well as functional rescue experiments by reintroducing CD2AP variants. Downstream readouts such as RT-qPCR and flow cytometry for surface receptors (e.g., integrins) allow detailed molecular phenotyping. For comprehensive technical protocols and inquiries, please contact Ascent Research.
