The EHD1 Knockout A2780 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian adenocarcinoma cell line. This heterogeneous pool of cells carries targeted disruptions in the EHD1 gene, providing a robust loss-of-function model for studying EHD1-dependent processes in an ovarian cancer background. The polyclonal format minimizes clonal bias and is ideal for population-based assays such as receptor recycling and migration studies.
The A2780 cell line originates from an untreated patient with ovarian carcinoma and displays adherent epithelial morphology. Widely used in ovarian cancer research, these cells retain key malignant features, including dysregulated signaling and migratory properties. Their well-characterized nature and ease of culture make them a suitable host for CRISPR knockout experiments aimed at dissecting molecular pathways in tumor biology. In the context of EHD1 disruption, A2780 cells provide a relevant platform to evaluate how endocytic recycling influences ovarian cancer cell behavior.
EHD1 is an ATPase that drives endocytic recycling by mediating membrane fission on endosomes. Following ATP hydrolysis, EHD1 oligomerizes and collaborates with Rab11, Rab8, Syndapin2, and MICAL-L1 to sever tubules and promote vesicle formation. This activity recycles internalized receptors, such as integrins and the transferrin receptor, back to the plasma membrane, thereby regulating surface receptor levels and downstream events like actin polymerization and cell migration. EHD1 also participates in ciliary membrane protein trafficking, linking it to ciliogenesis. Its function is modulated by Rab GTPases, membrane phospholipids like PI(4,5)P2, and membrane curvature.
In ovarian carcinoma, EHD1-mediated receptor trafficking controls the surface expression of integrins, which are critical for adhesion, invasion, and metastasis. Disrupting EHD1 in A2780 cells allows investigation of how altered recycling impacts cancer cell motility and drug sensitivity. Moreover, EHD1??s role in ciliogenesis suggests potential crosstalk with ciliopathy-related pathways that may influence ovarian tumorigenesis. This model thus serves as a powerful tool to explore the intersection of endocytic trafficking and ovarian cancer progression, guiding the identification of therapeutic targets within the recycling machinery.
These polyclonal knockout cells are compatible with diverse experimental approaches, including transferrin uptake and recycling assays to measure endocytic kinetics, flow cytometry for surface receptor quantification, and migration/invasion assays to evaluate metastatic potential. The model can be used in co-immunoprecipitation to probe EHD1 protein interactions and in RNA-seq to uncover transcriptomic alterations. Ciliogenesis studies can assess defects in ciliary protein trafficking upon EHD1 loss. For additional product details or custom service inquiries, please contact Ascent Research.
