The CC2D1A Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma epithelial cell line. This gene-edited product features disruption of the CC2D1A gene, which encodes a transcriptional repressor involved in critical cellular processes. The polyclonal format provides a heterogeneous population of knockout cells, suitable for studying gene function without the constraints of clonal selection. The genetic modification was achieved using CRISPR/Cas9-mediated gene disruption, resulting in a loss-of-function model for CC2D1A.
The parental A2780 cell line was originally established from an untreated ovarian carcinoma patient, serving as a widely used model for ovarian cancer biology. A2780 cells exhibit epithelial morphology and are commonly employed in studies of tumorigenesis, drug resistance, and signaling pathway dysregulation. This host line retains key characteristics of ovarian cancer, making it a relevant system for investigating the impact of CC2D1A depletion on oncogenic phenotypes.
CC2D1A functions as a transcriptional repressor that recruits histone deacetylases (HDACs) to silence gene expression, negatively regulating NF-kappaB signaling through direct interaction with NF-kappaB subunits such as RELA and NFKB1. It inhibits the transcriptional activity of NF-kappaB, thereby modulating downstream targets including CREB and NF-kappaB-responsive genes. CC2D1A operates within a network involving upstream NF-kappaB pathway components like IKBKB and CHUK, and intersects with Wnt signaling via DVL and GSK3B. Additionally, CC2D1A associates with chromatin remodelers, influencing endosomal trafficking and inflammatory responses.
In the A2780 ovarian cancer context, loss of CC2D1A can alter NF-kappaB activity, a pathway frequently deregulated in ovarian carcinomas, contributing to proliferation, survival, and therapeutic resistance. This knockout model enables dissection of CC2D1A’s role in modulating oncogenic signaling, apoptosis, and the inflammatory tumor microenvironment. By disrupting a key repressor, researchers can probe the consequences of enhanced NF-kappaB signaling in epithelial ovarian cancer cells.
Typical applications include functional studies of CC2D1A in ovarian cancer pathogenesis, dissection of NF-kappaB regulatory mechanisms, and investigation of cross-talk with Wnt signaling. End-users can validate knockout efficacy via RT-qPCR and Western blotting, and assess pathway activity using NF-kappaB luciferase reporter assays. Functional assays such as apoptosis and proliferation analyses provide insight into cellular outcomes following gene disruption. This product is suitable for drug screening campaigns targeting NF-kappaB or chromatin-modifying enzymes, and for neurobiology research exploring intellectual disability and autism spectrum disorder mechanisms. For further details or technical assistance, please contact Ascent Research.
