The CCDC25 knockout MES-OV polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian endometrioid carcinoma cell line MES-OV. This genetic disruption targets the CCDC25 gene, generating a loss-of-function model suitable for investigating CCDC25-mediated signaling pathways. The polyclonal format provides a heterogeneous pool of edited alleles, enabling robust functional studies without clonal bias.
MES-OV is a well-characterized epithelial ovarian cancer cell line established from a patient tumor, representing a clinically relevant model for endometrioid ovarian carcinoma. It retains key features of ovarian cancer biology, including invasive and metastatic properties, making it an ideal host for studying mechanisms of tumor dissemination, particularly to the peritoneal cavity and liver.
CCDC25 functions as a single-pass transmembrane receptor that senses extracellular DNA released from neutrophil extracellular traps (NETs). Upon binding its ligand, CCDC25 engages and activates integrin-linked kinase (ILK), which directly phosphorylates ??-parvin. This activation precipitates a cascade of actin cytoskeleton reorganization and focal adhesion turnover, mediated by downstream effectors including focal adhesion kinase (FAK) and Rho GTPases. The CCDC25-ILK-??-parvin signaling axis is further modulated by upstream regulators such as NET-derived DNA, HMGB1, and neutrophil elastase, and is integrated with the PAR complex and integrin-mediated adhesion dynamics. Through these interactions, CCDC25 links extracellular NET signals to intracellular motility programs that drive tumor cell migration and invasion.
In the MES-OV ovarian cancer model, CCDC25 is a critical transducer of NET-induced metastasis, a process implicated in peritoneal carcinomatosis and liver metastasis. Disrupting CCDC25 in this context allows precise dissection of how NETosis signaling contributes to ovarian cancer progression. The knockout cells provide a clean genetic background to interrogate the ILK-??-parvin pathway and its role in actin-driven cell motility, independent of compensatory mechanisms. This model is particularly valuable for validating CCDC25 as a therapeutic target and for probing crosstalk between inflammatory microenvironments and metastatic signaling.
These polyclonal knockout cells are suited for a wide range of functional assays, including NET-stimulated transwell migration and invasion studies, co-immunoprecipitation of ILK to assess receptor complex formation, and western blot analysis of ??-parvin phosphorylation. Immunofluorescence staining for F-actin and focal adhesion markers such as paxillin can be combined with inhibitor treatments to screen for small molecules targeting the CCDC25-ILK interface. The model also supports in vivo mouse metastasis experiments to evaluate the impact of CCDC25 loss on peritoneal spread or hepatic colonization. For further information or to discuss custom applications, please contact Ascent Research.
