EHD4 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian carcinoma cell line A2780. This product provides a genetically disrupted pool of cells with loss-of-function of the EHD4 gene, enabling investigation of endocytic recycling-dependent processes in an ovarian cancer context. The polyclonal format ensures a heterogeneous knockout population, preserving biological variability while allowing robust functional studies. This model is suitable for researchers studying receptor trafficking, cell migration, and drug response mechanisms in ovarian carcinoma.
The parental A2780 cell line is a well-characterized human ovarian carcinoma model established from an untreated patient. A2780 cells are widely used in biomedical research to study ovarian cancer biology, including mechanisms of drug sensitivity and resistance, cell signaling, and tumor progression. Their epithelial origin and defined genetic background make them a reliable system for interrogating gene-specific functions in cancer-relevant pathways. The A2780 line is particularly valued for its responsiveness to platinum-based chemotherapeutics, providing a relevant platform for investigating molecular determinants of treatment outcomes.
EHD4 encodes an endocytic recycling GTPase that orchestrates the return of internalized plasma membrane receptors and integrins to the cell surface. It functions within a network involving upstream regulators such as EGF, Src kinase, and Rab5, and directly interacts with Rabenosyn-5, Syndapin, Arf6, and MICAL-L1 to facilitate endosomal sorting and recycling. Through these interactions, EHD4 modulates the trafficking of key receptors including EGFR and integrins, thereby influencing actin cytoskeleton remodeling and cell migration. Its activity is integrated with Rac1 signaling, highlighting a role in coordinating membrane dynamics with cell motility. Disruption of EHD4 expression leads to impaired recycling of these receptors, which can attenuate downstream signaling cascades.
In A2780 ovarian cancer cells, loss of EHD4 disrupts EGFR and integrin recycling, potentially impairing cell migration and proliferation. This model enables dissection of how endocytic trafficking contributes to ovarian carcinoma cell behavior, including responses to growth factors and chemotherapeutic agents. By studying polyclonal EHD4 knockout cells, researchers can evaluate the collective impact on receptor tyrosine kinase signaling, integrin-mediated adhesion, and invasive potential without clonal artifacts. This system is particularly relevant for exploring mechanisms of drug resistance, as altered receptor trafficking is often implicated in the acquisition of resistance to targeted therapies and platinum-based drugs.
This product can be applied in a range of experimental approaches, including western blotting, RT-qPCR, migration and invasion assays, EGFR recycling assays, immunofluorescence, flow cytometry, co-immunoprecipitation, and phospho-signaling analysis. These tools allow comprehensive characterization of endocytic trafficking phenotypes and their downstream effects on oncogenic signaling. Researchers can use the polyclonal knockout population to screen for functional changes resistant to clonal variation, or to isolate subpopulations with distinct trafficking behaviors. The cells also serve as a valuable control for EHD4 re-expression experiments or drug response studies. For more details or technical support, please contact Ascent Research.
