This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, with targeted disruption of the CCDC82 gene. The polyclonal format provides a heterogeneous pool of edited cells, avoiding clonal selection biases and enabling unbiased functional studies.
The A2780 cell line is a well-characterized epithelial ovarian carcinoma model established from an untreated patient. It exhibits cisplatin sensitivity, carries a p53 mutation, and retains wild-type BRCA1 and BRCA2. This line is extensively employed to study mechanisms of chemoresistance, oncogenic signaling, and tumor biology in ovarian cancer.
CCDC82 encodes a coiled-coil domain protein that negatively regulates NF-??B signaling by directly binding and inhibiting IKK?? kinase activity. Under basal conditions, this interaction suppresses phosphorylation of I??B??, preventing NF-??B (p65/p50) nuclear translocation and target gene transcription. Upon stimulation by upstream signals such as TNF?? and IL-1??, CCDC82 restrains pathway output; its loss unleashes IKK?? activity, leading to upregulated expression of downstream effectors including IL-6, IL-8, TNF??, BCL2, BCL-xL, cyclin D1, and c-Myc.
In the A2780 background, CCDC82 loss results in sustained NF-??B pathway activation, even in the absence of strong exogenous stimuli, boosting expression of proliferative and anti-apoptotic genes. This heightened signaling is particularly relevant for studying ovarian cancer drug resistance, as NF-??B can promote survival under genotoxic stress. The combination of a TP53 mutation and constitutive NF-??B activity mirrors aggressive disease features, making this a compelling model for therapeutic target validation.
This knockout model enables a wide range of functional studies, including dissection of NF-??B regulatory circuits, identification of synthetic lethal interactions in ovarian cancer, and mechanistic investigation of cisplatin sensitivity. Researchers can utilize techniques such as western blotting to monitor phospho-p65 (Ser536) and I??B?? degradation, RT-qPCR for NF-??B target genes (e.g., IL6, BCL2), dual-luciferase NF-??B reporter assays, immunofluorescence to track p65 nuclear translocation, and flow cytometry for Annexin V-based apoptosis detection. Co-immunoprecipitation can verify the loss of CCDC82?CIKK?? interaction, while cisplatin dose?Cresponse and migration assays assess functional consequences. These polyclonal knockout cells are also well-suited for arrayed or pooled CRISPR screens. For additional details or to discuss specific research applications, please contact Ascent Research.
