The CCDC102A Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CCDC102A gene in the human MES-OV ovarian carcinoma cell line. This heterogeneous knockout model provides a loss-of-function system for studying the poorly characterized coiled-coil domain-containing protein CCDC102A, without the clonal biases inherent in single-cell-derived knockouts. The polyclonal format ensures a broad spectrum of edited alleles, enabling population-level functional analyses of gene disruption effects.
The MES-OV cell line is a widely used human epithelial ovarian cancer model derived from a high-grade serous adenocarcinoma. It belongs to the mesenchymal molecular subtype, characterized by fibroblast-like morphology, elevated expression of mesenchymal markers such as vimentin and N-cadherin, and enhanced migratory and invasive capabilities. This subtype is clinically associated with platinum resistance and poor patient outcomes, making MES-OV a valuable model for studying ovarian cancer aggressiveness, epithelial-to-mesenchymal transition, and metastatic dissemination.
CCDC102A encodes a coiled-coil domain-containing protein predicted to localize to centrosomes. Although its precise functions remain undefined, it may associate with ??-tubulin, a key microtubule nucleating factor, and with CEP family proteins that regulate centriole duplication and elongation. These interactions suggest a role in centrosome maturation and microtubule organization, potentially influencing cell cycle progression, mitotic spindle assembly, and chromosome segregation. Dysregulation of centrosome biology is a common feature of many cancers, contributing to genomic instability, and thus characterizing such centrosome-associated proteins is critical.
In the context of the MES-OV mesenchymal ovarian cancer model, disruption of CCDC102A offers a unique opportunity to probe centrosome-dependent vulnerabilities. Mesenchymal ovarian cancers often exhibit heightened genomic instability and aggressive behavior; perturbing a candidate centrosomal regulator may alter cell cycle checkpoints, proliferation, apoptosis, and invasive capacity. This model allows researchers to dissect how loss of CCDC102A intersects with mesenchymal signaling networks to impact tumor cell fitness and drug sensitivity, particularly to microtubule-targeting chemotherapies such as taxanes.
Standard applications include Western blotting, RT-qPCR, immunofluorescence microscopy for centrosome analysis, flow cytometry for cell cycle and apoptosis profiling, and migration/invasion assays using transwell systems. Drug sensitivity testing against chemotherapeutic agents can reveal vulnerabilities induced by CCDC102A loss. These methodologies collectively enable elucidation of CCDC102A function and its therapeutic potential in ovarian cancer. For further details, please contact Ascent Research.
