The DTNBP1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DTNBP1 gene in the MES-OV human ovarian adenocarcinoma cell line. This loss-of-function model eliminates dysbindin-1 expression, providing a heterogeneous cell pool to study the consequences of DTNBP1 deficiency without clonal isolation.
MES-OV is a mesenchymal-subtype ovarian cancer cell line characterized by enhanced migratory and invasive properties, serving as a model for aggressive, chemoresistant disease. Its mesenchymal features make it ideal for investigating lysosomal remodeling and drug resistance mechanisms in ovarian cancer.
DTNBP1 encodes dysbindin-1, a core subunit of the BLOC-1 complex that governs endosomal cargo sorting and lysosome-related organelle biogenesis. Dysbindin-1 interacts with BLOC1S1?CBLOC1S6, DTNA, DTNB, SNARE proteins, and the AP-3 adaptor complex, working downstream of TFEB and SNARE regulators to direct lysosomal enzymes and synaptic vesicle proteins. Disruption of DTNBP1 impairs lysosomal trafficking and endosomal sorting, contributing to pathologies such as Hermansky-Pudlak syndrome type 7 and schizophrenia.
In MES-OV cells, DTNBP1 ablation allows exploration of the link between lysosomal dysfunction and ovarian cancer aggression. Impaired BLOC-1 function may underlie the aberrant lysosomal sequestration of chemotherapeutics, a key mechanism of drug resistance. This knockout model enables dissection of dysbindin-1??s role in autophagy, cell migration, and invasion, and how endosomal sorting regulates metastasis-related signaling.
The DTNBP1 Knockout MES-OV Polyclonal Cells support diverse assays including western blotting for BLOC-1 subunits, immunofluorescence for LAMP1/2, lysosomal pH measurement, and confocal analysis of endosomal trafficking. RT-qPCR quantifies lysosomal biogenesis genes, while chemosensitivity and migration assays reveal functional impacts. RNA-seq can uncover global transcriptional changes. For inquiries, contact Ascent Research.
