The CCDC138 Knockout A2780 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of A2780 ovarian carcinoma cells with targeted disruption of the CCDC138 gene. CCDC138 encodes a coiled-coil domain-containing protein whose function remains poorly understood. Because the knockout pool comprises a heterogeneous mix of edited alleles, it avoids the confounding effects of clonal selection and offers a more representative loss-of-function model for functional genomics studies. This product is designed to facilitate the exploration of CCDC138’s role in cancer cell biology through comparative analyses with wild-type controls.
The A2780 cell line originated from an untreated patient with high-grade serous ovarian carcinoma and is widely used as a cisplatin-sensitive model of the disease. It retains characteristics of ovarian tumor epithelium and supports reproducible experimental results, making it a reliable platform for investigating oncogenic mechanisms and drug responses. By introducing the CCDC138 knockout into this well-characterized line, the product provides a clinically relevant context for studying the gene’s influence on ovarian cancer pathology.
CCDC138 is classified as a coiled-coil domain-containing protein, a structural motif frequently associated with protein-protein interactions and macromolecular complex assembly. Despite this, no specific binding partners, upstream activators, or downstream effectors of CCDC138 have been identified, and its signaling network remains uncharted. The knockout model thus serves as a critical tool for de novo discovery of CCDC138’s molecular connections and functional contributions. It is hypothesized that loss of CCDC138 may disrupt putative interaction networks, potentially altering cellular behaviors such as proliferation, survival, or motility, though the precise mechanistic outcomes are yet to be determined.
Engineering the CCDC138 knockout in A2780 cells enables targeted investigation of the gene’s role in ovarian cancer biology. Given the line’s cisplatin sensitivity, the model is particularly valuable for assessing how CCDC138 loss modulates chemotherapeutic response, cell death pathways, and metastatic potential. Comparative studies with wild-type A2780 cells can uncover functions of CCDC138 in processes like DNA damage repair, cell cycle control, or apoptosis. The polyclonal population format further ensures that observed phenotypes are not artifacts of single-clone adaptation, yielding more generalizable insights.
These polyclonal knockout cells are suited for diverse assays, including proliferation, apoptosis, migration/invasion, colony formation, and drug sensitivity testing. Molecular analyses such as western blotting, RT-qPCR, and immunofluorescence can validate knockout and probe downstream effects. The model also supports proteomic screening to identify novel CCDC138 interactors and pathway mapping. Through such applications, researchers can advance the understanding of CCDC138 in ovarian cancer and explore its potential as a therapeutic target. For additional information or custom requests, please contact Ascent Research.
