The DPYSL5 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the MES-OV human ovarian cancer mesenchymal cell line. This polyclonal format provides a heterogeneous knockout model suitable for studying loss-of-function effects of the DPYSL5 gene, which encodes collapsin response mediator protein 5 (CRMP5). The pool contains a diverse array of CRISPR/Cas9-mediated gene disruptions across the cell population, offering a robust system to interrogate DPYSL5-dependent phenotypes without the clonal selection artifacts inherent to single-cell-derived lines.
MES-OV is an established human ovarian cancer cell line derived from a malignant mixed mesodermal tumor, exhibiting a characteristic mesenchymal phenotype. This cell line is widely used as a model for aggressive ovarian cancer with mesenchymal differentiation, featuring enhanced migratory and invasive properties. Its mesenchymal background makes it particularly relevant for investigating the molecular mechanisms governing epithelial-to-mesenchymal transition (EMT) and metastatic dissemination, processes central to ovarian cancer progression.
DPYSL5 (CRMP5) is a member of the CRMP family of phosphoproteins that regulate microtubule dynamics and signal transduction during axon guidance and neuronal polarity. CRMP5 promotes microtubule assembly by directly binding tubulin heterodimers. Its activity is modulated by phosphorylation cascades downstream of Semaphorin 3A (Sema3A)/plexin and Reelin/Dab1 signaling; kinases including Fyn, Cdk5, and GSK3?? phosphorylate CRMP5, altering its interaction with tubulin heterodimers and the actin cytoskeleton. CRMP5 also interacts with other CRMP family members (DPYSL2/CRMP2, DPYSL3/CRMP4) and ??-actinin, thereby contributing to coordinated regulation of cytoskeletal rearrangement essential for cell migration and neurite outgrowth.
In the MES-OV mesenchymal ovarian cancer context, DPYSL5 disruption is predicted to impact microtubule polymerization and cell migration capacity. Given the gene??s established roles in axon guidance and neuronal differentiation, this knockout model allows researchers to dissect its non-neuronal functions in tumor cell motility and invasion. The mesenchymal nature of MES-OV cells, combined with CRMP5??s involvement in cytoskeletal dynamics, makes this polyclonal population an ideal tool to study how semaphorin and Reelin signaling pathways intersect with ovarian cancer metastatic behavior. Additionally, DPYSL5 has been associated with neuroendocrine tumor differentiation, providing a platform to explore its contribution to tumor phenotype plasticity.
This knockout cell pool supports diverse research applications, including ovarian cancer metastasis studies, microtubule dynamics assays, and neuroendocrine differentiation investigations. Representative assays to validate knockout effects include western blotting for DPYSL5 and its phosphorylated forms, transwell migration and invasion assays, and microtubule polymerization assays. Immunofluorescence staining for tubulin can visualize cytoskeletal changes, while RNA-seq transcriptomic profiling captures downstream gene expression alterations. The cells are also amenable to drug sensitivity testing with chemotherapeutics, aiding target screening efforts. For further details or technical support, please contact Ascent Research.
