EID2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, designed for the targeted disruption of the EID2 gene. This product offers a powerful loss-of-function model for investigating the role of EID2 in transcriptional repression and cancer biology. The polyclonal format provides a heterogeneous pool of cells with diverse editing outcomes, enabling robust population-level studies without clonal selection bias.
The A2780 cell line is an epithelial ovarian carcinoma model established from an untreated patient, widely utilized in oncology research for studying tumor biology, signaling pathways, and drug responses. These cells retain key molecular features of ovarian cancer, including intact retinoic acid signaling and functional p53, making them a relevant context for examining the epigenetic and transcriptional mechanisms controlled by EID2. Their adherent growth and well-characterized genetic background facilitate reproducible experimental workflows.
EID2 (EP300-interacting inhibitor of differentiation 2) functions as a transcriptional corepressor by binding to EP300 and CREBBP and inhibiting their histone acetyltransferase (HAT) activity. This inhibition results in decreased acetylation of histones and non-histone proteins, leading to the repression of genes critical for cellular differentiation and tumor suppression. The EID2 regulatory network is directly linked to retinoic acid signaling, where RAR/RXR transcription factors activate EID2 expression. Downstream, reduced EP300/CREBBP activity modulates p53 function and diminishes the expression of target genes involved in cell cycle arrest and apoptosis. Representative pathway components include EP300, CREBBP, acetylated histones, and the general transcriptional machinery.
In the A2780 ovarian carcinoma context, EID2 knockout disrupts a key node in the epigenetic control of gene expression, potentially altering the balance between differentiation and proliferation. Loss of EID2-mediated repression is expected to enhance histone acetylation at EP300/CREBBP target loci, derepressing genes that may counteract tumorigenic phenotypes. This model is particularly relevant for exploring how epigenetic regulators influence ovarian cancer cell fate, drug sensitivity, and the cellular response to retinoic acid or histone deacetylase inhibitors. It also provides a platform to study interactions between EID2 and the p53 pathway in a cancer cell line with wild-type p53 status.
Researchers can utilize this knockout model in a variety of applications, including Western blotting to assess EID2 and acetylated histone levels, RT-qPCR or RNA-seq to profile transcriptomic changes, and proliferation assays (MTT, BrdU) to evaluate growth effects. Additional assays such as flow cytometry for cell cycle and apoptosis analysis, drug sensitivity testing with cisplatin, and ChIP-qPCR for histone acetylation at specific promoters are well-suited to dissect EID2 function. This product is an essential tool for functional genomics of epigenetic regulators, cancer differentiation studies, and drug resistance research. For detailed technical specifications or ordering information, please contact Ascent Research.
