The DNAJC6 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian cancer cell line, engineered to disrupt the DNAJC6 gene. This heterogeneous pool provides a loss-of-function model for studying auxilin-dependent cellular processes, with the polyclonal format offering a robust and representative population for downstream analyses.
The MES-OV cell line originates from a human ovarian adenocarcinoma and exhibits a mesenchymal morphology, making it a widely used model for investigating ovarian cancer metastasis, epithelial-mesenchymal transition (EMT), and drug resistance. Its mesenchymal characteristics facilitate studies of cell migration, invasion, and plasticity, relevant to aggressive cancer phenotypes.
DNAJC6 encodes auxilin, a neuronal J-domain co-chaperone that recruits Hsc70 (HSPA8) to clathrin-coated vesicles, driving clathrin lattice disassembly and vesicle uncoating after endocytosis. This process is essential for recycling synaptic vesicles and receptors. Auxilin interacts with clathrin heavy chain and the AP-2 adaptor complex, and its activity is regulated by PACSIN proteins and neuronal activity. Downstream, auxilin-mediated uncoating promotes early endosome formation, receptor recycling, and signaling attenuation. The clathrin-mediated endocytosis pathway includes clathrin triskelion, AP2 adaptor, Hsc70 co-chaperone, and accessory proteins like synaptojanin 1.
In ovarian cancer cells, clathrin-mediated endocytosis governs internalization of growth factor receptors such as EGFR, thereby modulating signal transduction, proliferation, and migration. Disruption of DNAJC6 in the MES-OV background may impair clathrin uncoating, leading to altered receptor trafficking and signaling dynamics. This model enables dissection of auxilin??s non-neuronal roles in endocytic regulation within a mesenchymal cancer context, potentially linking endocytic dysfunction to EMT and drug resistance mechanisms.
The DNAJC6 Knockout MES-OV Polyclonal Cells are suitable for investigating clathrin-mediated endocytosis, auxilin function in ovarian cancer, receptor trafficking, and signal transduction. Researchers can employ western blotting to assess auxilin levels, immunofluorescence to visualize clathrin dynamics, transferrin uptake and EGFR internalization assays to quantify endocytosis, co-immunoprecipitation to study interactions with Hsc70, and flow cytometry to measure surface receptor expression. Transcriptomic analyses via RT-qPCR or RNA-seq can further elucidate DNAJC6-dependent pathways. For technical support or ordering information, please contact Ascent Research.
