The DNM1 Knockout MES-OV Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of MES-OV ovarian epithelial cells carrying targeted disruptions in the DNM1 gene. This mixed-cell knockout model provides a versatile system for studying dynamin-1 function in endocytosis and downstream signaling pathways in an ovarian cancer context, without clonal bias.
The MES-OV cell line, derived from a human ovarian endometrioid adenocarcinoma, is a standard model for gynecological cancer research. As epithelial cells, they retain key characteristics of ovarian endometrioid carcinoma, making them well-suited for investigating membrane trafficking events that influence growth factor receptor signaling and tumor cell behavior.
DNM1 encodes dynamin-1, a large GTPase essential for membrane scission during clathrin-mediated endocytosis. Dynamin-1 is activated by upstream kinases such as EGF receptor signaling, c-Src, CaMKII, and PKC, and it interacts with Amphiphysin 1, Endophilin A1, SNX9, Clathrin heavy chain, Cortactin, and Actin. Its primary function is to liberate endocytic vesicles, enabling internalization of receptor tyrosine kinases like EGFR and HER2. This internalization governs the strength and duration of MAPK and AKT signaling pathways, directly linking endocytosis to cell proliferation and survival decisions.
Knockout of DNM1 in MES-OV cells blocks efficient EGFR uptake, leading to attenuated MAPK and AKT pathway activation and potentially reduced tumor cell proliferation and migration. This polyclonal knockout population captures the natural variability of endocytic dependency across ovarian cancer cells, offering a more representative model than single-strain clonal knockouts for studying endocytosis-driven signaling and for therapeutic target validation.
Researchers can apply this model in western blotting to assess changes in phosphorylated EGFR, ERK, and AKT; immunofluorescence to visualize clathrin-coated pits and cargo internalization; and functional assays such as transferrin uptake or EGFR internalization kinetics. Additional techniques include cell migration and invasion assays to evaluate metastatic potential, RNA-seq for transcriptomic profiling, and co-immunoprecipitation to map dynamin-1 interactomes. For further information, please contact Ascent Research.
