The CCDC90B Knockout A2780 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of A2780 human ovarian carcinoma epithelial cells with targeted disruption of the CCDC90B gene. This loss-of-function model was generated using CRISPR/Cas9 gene editing to introduce targeted disruptions in the coding sequence, resulting in a heterogeneous knockout cell pool. The polyclonal format avoids clonal selection, maintaining genetic diversity that can be beneficial for studying gene function in a population context and reducing potential clonal artifacts. The knockout is designed to eliminate CCDC90B protein expression, enabling researchers to investigate the cellular consequences of its loss in a cancer-relevant setting.
The A2780 cell line is a well-characterized epithelial ovarian carcinoma model, originally derived from an untreated patient with ovarian endometrioid adenocarcinoma. It is extensively utilized in ovarian cancer research due to its ability to recapitulate key aspects of tumor biology, including dysregulated growth signaling, drug sensitivity profiles, and metastatic properties. A2780 cells serve as a robust platform for functional genomics studies, providing a reproducible system for dissecting the molecular pathways that drive ovarian cancer progression and therapeutic response.
CCDC90B encodes a protein featuring a coiled-coil domain, a structural motif known to mediate protein-protein interactions. Although its biological function remains poorly defined, the presence of this domain suggests CCDC90B may function as a scaffold or adaptor, facilitating interactions with other coiled-coil-containing proteins. The mechanistic consequence of CCDC90B knockout is hypothesized to disrupt these interaction networks, potentially altering downstream processes such as cell cycle progression, apoptosis, or cytoskeletal dynamics. To date, no specific upstream regulators, downstream targets, or direct binding partners have been validated; however, the coiled-coil architecture implicates involvement in supramolecular complexes essential for cellular homeostasis.
In the context of A2780 ovarian carcinoma cells, CCDC90B knockout provides a valuable tool to dissect the gene??s contributions to cancer cell biology. By eliminating CCDC90B expression, researchers can assess changes in proliferation, chemosensitivity, invasive capacity, and global gene expression profiles. Given the limited characterization of CCDC90B, this model may uncover novel roles in ovarian tumorigenesis, such as modulation of epithelial-mesenchymal transition or DNA damage response. Thus, the knockout cells enable the functional annotation of a previously uncharacterized coiled-coil protein in a disease-relevant model.
This product is ideally suited for a comprehensive suite of downstream applications, including quantitative expression analysis by RT-qPCR, protein verification via Western blotting, and functional assays such as MTS or colony formation for proliferation, Annexin V staining for apoptosis, flow cytometric cell cycle profiling, and Transwell migration/invasion assessments. Global transcriptome analysis by RNA-seq can be employed to identify downstream targets and regulatory networks affected by CCDC90B loss. Additionally, these cells support drug response screens to evaluate sensitivity to standard-of-care chemotherapeutics or targeted agents. For further technical details or assistance, please contact Ascent Research.
