The DYNC1LI1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population carrying targeted disruption of the DYNC1LI1 gene. Derived from the MES-OV human ovarian cancer cell line, this product provides a heterogeneous loss-of-function model to study cytoplasmic dynein light intermediate chain 1 function in a mesenchymal tumor background. The polyclonal format avoids clonal selection bias, enabling robust population-level phenotypic analyses.
MES-OV is a high-grade serous ovarian carcinoma cell line with a mesenchymal molecular subtype and epithelial-mesenchymal transition (EMT) features. It displays aggressive migratory and invasive behavior and intrinsic chemoresistance, serving as a model for metastatic ovarian cancer. This cellular context is ideal for investigating genes that regulate cytoskeletal dynamics and intracellular trafficking in therapy-resistant tumors.
DYNC1LI1 encodes LIC1, a light intermediate chain of cytoplasmic dynein, which links the motor complex to cargoes such as late endosomes, Golgi, mitochondria, and EGFR. Its activity is modulated by dynactin, BicD2, LIS1, NDE1, and CDK5 phosphorylation. DYNC1LI1 is essential for retrograde transport, mitotic spindle assembly, Golgi organization, and cell migration. Knockout disrupts these processes, impairing organelle positioning and mitotic fidelity.
In MES-OV cells, DYNC1LI1 loss compromises dynein-dependent transport pathways that support invasion and drug tolerance. Disruption may affect EGFR trafficking, mitotic checkpoint signaling, and polarized organelle distribution required for mesenchymal migration. Thus, this knockout model enables investigation of how dynein-mediated intracellular logistics contribute to ovarian cancer aggressiveness and chemoresistance.
Applications include western blot and immunofluorescence to verify knockout efficiency and subcellular dynein distribution, migration/invasion assays, drug sensitivity profiling, organelle positioning analysis, mitotic index measurement, and RNA-seq transcriptomics. These polyclonal cells are suited for synthetic lethality screens and mechanistic studies of microtubule motor-dependent signaling in malignancy. For inquiries, please contact Ascent Research.
