The DNM1 Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNM1 gene has been functionally disrupted to generate a loss-of-function model. This product is supplied as a heterogeneous pool of A2780 cells harboring diverse CRISPR/Cas9-induced mutations at the target locus, providing a robust platform for studying dynamin-1 deficiency without clonal artifacts. The polyclonal format enables assessment of overall gene function while maintaining genetic diversity representative of the edited population.
The parental A2780 cell line is a well-characterized human ovarian carcinoma epithelial model established from an untreated patient with ovarian endometrioid adenocarcinoma. These adherent cells retain cisplatin sensitivity and are widely employed to investigate ovarian cancer biology, including tumorigenesis, metastasis, and chemotherapeutic response. Their epithelial morphology and genetic background make them suitable for studies of receptor trafficking and cell migration in a cancer-relevant context.
Dynamin-1, encoded by DNM1, is a large GTPase critical for membrane fission during clathrin-mediated endocytosis. It self-assembles into helical collars at the necks of budding vesicles and undergoes GTP hydrolysis-driven conformational changes to mediate vesicle scission. The protein functions downstream of EGFR activation and is regulated by kinases such as GSK3?? and CDK5, and by the phosphatase calcineurin. It directly interacts with scaffold proteins including Amphiphysin, Endophilin, SNX9, Intersectin, and Syndapin, and cooperates with the AP2 complex and Clathrin for cargo internalization. Upon disruption, receptor internalization is impaired, leading to altered endosomal signaling via Akt and ERK pathways and defective downregulation of surface receptors.
In the A2780 background, loss of dynamin-1 disrupts clathrin-mediated internalization of receptors critical for ovarian cancer progression, such as EGFR. This impairment is expected to attenuate downstream oncogenic signaling cascades and may compromise processes like cell migration and invasion driven by integrin trafficking and focal adhesion dynamics. Given the cisplatin sensitivity of A2780 cells, this knockout model offers a unique system to dissect how endocytic trafficking influences chemotherapeutic response and metastatic potential in ovarian carcinoma.
This polyclonal knockout cell population is suitable for diverse applications, including investigation of dynamin-1??s role in ovarian cancer endocytosis and metastasis, functional analysis of clathrin-mediated internalization in cancer signaling, drug delivery and nanoparticle uptake studies, and screening of dynamin inhibitors. Recommended assays include Western blotting for DNM1, transferrin-Alexa Fluor uptake, EGFR internalization and degradation kinetics, scratch wound healing, and phospho-Akt/phospho-ERK Western blot. For further information and to discuss your specific needs, please contact Ascent Research.
