The CCDC71L Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CCDC71L gene in the MES-OV human ovarian clear cell carcinoma cell line. This polyclonal loss-of-function model, generated via CRISPR/Cas9-mediated gene disruption, provides a heterogeneous knockout pool that avoids clonal selection artifacts, better recapitulating tumor heterogeneity for functional studies.
The MES-OV host line, derived from human ovarian clear cell carcinoma, displays a pronounced mesenchymal phenotype with high migratory and invasive capacity, making it a well-established model for epithelial-mesenchymal transition (EMT) and metastasis research. Its genetic background offers a clinically relevant system for studying tumor suppressors in aggressive ovarian cancer.
CCDC71L encodes a coiled-coil domain protein that acts as a putative tumor suppressor by inhibiting cell proliferation and invasion. Its loss leads to dysregulation of PI3K/AKT/mTOR and MAPK/ERK pathways, resulting in upregulation of EMT transcription factors Snail and Zeb1, reduced epithelial E-cadherin, and increased mesenchymal vimentin. Downstream, cell cycle regulators such as cyclins and CDKs are altered, promoting unchecked growth. CCDC71L is frequently silenced by promoter methylation, though its upstream transcriptional control remains poorly characterized.
In the MES-OV background, CCDC71L ablation accentuates the cell line??s innate mesenchymal and pro-metastatic properties, enabling dissection of its specific contribution to EMT and invasion. Comparative analyses of knockout and parental cells reveal enhanced EMT-related AKT and ERK signaling, driving a more aggressive phenotype. This model is particularly valuable for exploring the interplay between tumor suppressor loss and the mesenchymal state in ovarian carcinoma.
This polyclonal knockout pool supports diverse functional assays, including cell proliferation, transwell migration/invasion, and colony formation assays to quantify changes in growth and metastasis. Western blotting and RT-qPCR allow detailed profiling of EMT markers (Snail, vimentin, E-cadherin) and cell cycle proteins. RNA-seq can uncover global transcriptomic alterations, and immunofluorescence for cytoskeletal proteins reveals morphological changes. Apoptosis assays further assess survival. This tool is ideal for drug target validation and signaling pathway dissection. For further inquiries or custom services, please contact Ascent Research.
