The HDAC8 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian endometrioid adenocarcinoma cell line. This product contains a heterogeneous mix of cells with targeted disruption of the HDAC8 gene, providing a versatile loss-of-function model for studying HDAC8 biology. Unlike clonal lines, this polyclonal population captures the diversity of editing outcomes, suitable for pooled functional analyses.
The A2780 cell line represents a well-characterized model of ovarian endometrioid adenocarcinoma, originally isolated from an untreated patient. It is estrogen receptor-positive and widely employed in studies of ovarian cancer drug resistance and tumor progression. Its genetic and phenotypic features make it an ideal host for modeling the impact of HDAC8 loss in a disease-relevant context.
HDAC8 encodes a Class I histone deacetylase that catalyzes deacetylation of histones H3 and H4, promoting chromatin compaction and gene silencing. It also targets non-histone substrates including p53, SMC3, and the cohesion complex. HDAC8 is regulated by CDK1/cyclin B phosphorylation, PKA signaling, and caspase-3 cleavage, and it interacts with transcriptional corepressors such as SMRT/NCoR. Functionally, HDAC8 integrates signals from p53, Notch, TGF-??, Wnt, and estrogen pathways to control cell cycle progression and apoptosis. Its activity on p53 and cohesion components is critical for maintaining genomic stability in ovarian cancer cells.
In the A2780 ovarian cancer model, HDAC8 knockout disrupts these regulatory networks, leading to derepression of pro-apoptotic genes and cell cycle arrest. Loss of HDAC8-mediated p53 deacetylation enhances p53 transcriptional activity, increasing apoptosis and sensitizing cells to chemotherapeutic agents. Additionally, impaired deacetylation of SMC3 and RAD21 compromises cohesion function and DNA repair, further contributing to drug sensitivity. This makes the knockout model ideal for investigating HDAC8-dependent mechanisms of drug resistance and evaluating HDAC inhibitors such as vorinostat.
Applications include Western blotting for acetylation profiling, flow cytometry for apoptosis and cell cycle analysis, RT-qPCR for target gene expression, immunofluorescence for protein localization, co-immunoprecipitation for interaction studies, and HDAC activity assays. The polyclonal population is particularly suited for drug sensitivity assays (e.g., cisplatin, vorinostat) and HDAC inhibitor screening. This product supports research in ovarian cancer epigenetics, transcriptional regulation, and drug resistance. For additional details or customized editing services, please contact Ascent Research.
