The EHD3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, featuring targeted disruption of the EHD3 endocytic recycling protein. This heterogeneous knockout model provides a versatile tool for investigating the role of EHD3 in membrane trafficking and cancer biology, without the constraints of clonal selection. The polyclonal format is particularly suited for assays that assess population-averaged functional outcomes.
The A2780 cell line is a widely used epithelial ovarian carcinoma model, originally derived from an untreated patient with ovarian endometrioid adenocarcinoma. It is a cornerstone in ovarian cancer research for studying drug sensitivity and resistance mechanisms, owing to its well-characterized signaling profiles and responsiveness to chemotherapeutic agents. A2780 cells express relevant adhesion molecules and growth factor receptors, making them an ideal host for investigating how endocytic trafficking disruptions influence cancer cell behavior.
EHD3 is a member of the Eps15 homology domain protein family and functions as a dynamin-like ATPase essential for endocytic recycling. It regulates the return of internalized receptors and integrins from endosomes to the plasma membrane, a process activated by growth factors such as EGF and PDGF. EHD3 interacts with key trafficking regulators including Rab11, Arf6, and Eps15, and participates in Rab11-mediated recycling pathways. By controlling the surface availability of receptors like EGFR and integrins, EHD3 modulates downstream signaling cascades including AKT, focal adhesion kinase (FAK), and cell migration machinery. Loss of EHD3 disrupts this recycling, potentially leading to aberrant receptor accumulation, attenuated growth factor signaling, and reduced invasive capacity.
In the context of A2780 ovarian cancer cells, knockout of EHD3 is expected to impair the efficient recycling of growth factor receptors and integrins, which are often upregulated in ovarian cancer to sustain proliferation, migration, and therapy resistance. Consequently, these knockout cells may exhibit altered adhesion dynamics, reduced migration, and dampened AKT and ERK signaling, providing a model to dissect the contribution of endocytic trafficking to ovarian cancer progression. EHD3 has been implicated in multiple malignancies and other diseases, so these polyclonal cells also serve as a platform for cross-disease mechanistic studies.
Researchers can employ this model for a range of applications including immunofluorescence-based transferrin or EGFR recycling assays, Boyden chamber migration and invasion studies, and phospho-signaling analysis via western blot. Additionally, co-immunoprecipitation experiments can validate interactions between endogenous EHD3 and Rab11, and drug sensitivity profiling can uncover relationships between membrane protein turnover and chemotherapy response. Functional genomics screens further benefit from this knockout pool for probing endocytic regulators. For further information or technical assistance, please contact Ascent Research.
