The DYNLT1 Knockout MES-OV Polyclonal Cells are a heterogeneous population of CRISPR/Cas9-edited MES-OV cells carrying targeted disruption of the DYNLT1 gene. This polyclonal knockout product offers a robust loss-of-function model for investigating cytoplasmic dynein light chain Tctex-type 1 in a human ovarian clear cell carcinoma background. The use of CRISPR/Cas9-mediated gene disruption minimizes clonal bias and preserves population-level heterogeneity, making it suitable for studying general DYNLT1-dependent phenotypes.
MES-OV is a well-characterized human ovarian clear cell carcinoma cell line, serving as a clinically relevant model for this aggressive epithelial ovarian cancer subtype. Ovarian clear cell carcinoma frequently exhibits chemoresistance and distinct molecular features, and MES-OV cells retain key oncogenic signaling pathways operative in patient tumors. This cell line thus provides a pertinent context to examine the contributions of dynein-mediated transport to cancer cell biology.
DYNLT1 encodes a non-catalytic light chain subunit of the cytoplasmic dynein motor complex, which drives retrograde transport of diverse cargoes along microtubules. DYNLT1 directly interacts with the dynein heavy chain DYNC1H1 and the dynactin component DCTN1, and collaborates with cargo adaptors such as BICD2 and RAB6 to facilitate organelle positioning and mitotic spindle assembly. Its function integrates upstream cell cycle cues and downstream dynein cargo complexes, linking microtubule-based transport to processes including mitosis, intracellular trafficking, and cell cycle regulation. Within the dynein network, DYNLT1 operates alongside pathway components like LIS1, which modulates dynein motor activity. Disruption of DYNLT1 is expected to impair dynein-dependent retrograde transport, potentially affecting mitotic progression.
In the MES-OV ovarian cancer model, DYNLT1 knockout may compromise the efficient trafficking of mitotic regulators and signaling molecules, leading to aberrant cell division and altered viability. Ovarian clear cell carcinoma cells rely on robust intracellular transport for sustained proliferation and metastasis; thus, this knockout model enables dissection of DYNLT1??s role in cancer cell dynamics. By comparing wild-type and knockout polyclonal populations, researchers can assess changes in cell cycle distribution, migratory behavior, and response to therapeutic stress, providing insights into how dynein motor dysfunction influences ovarian cancer pathogenesis.
Researchers can employ this product in a wide range of functional assays, including western blotting and RT-qPCR for confirming target gene disruption, immunofluorescence to visualize dynein complex localization, and co-immunoprecipitation for mapping protein interaction networks. Cell-based applications extend to cell viability and proliferation measurements, transwell migration/invasion assays, and flow cytometric cell cycle analysis. This knockout model is particularly suited for studying dynein-mediated cargo trafficking in cancer, dissecting intracellular transport mechanisms, and advancing ovarian cancer pathophysiology research. For further information or technical support, please contact Ascent Research.
