The DNMT3A Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma epithelial cell line. This product contains a heterogeneous pool of cells with targeted disruption of the DNMT3A gene, generated via CRISPR/Cas9-mediated gene editing. The polyclonal format provides a diverse representation of knockout alleles, enabling robust loss-of-function studies without the need for single-cell cloning. This model serves as a valuable tool for investigating DNMT3A-dependent epigenetic regulation and its implications in cancer biology.
The A2780 cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and is widely used as a model for ovarian cancer research. These epithelial cells retain key characteristics of the original tumor, making them suitable for studying ovarian cancer pathogenesis, drug response, and epigenetic mechanisms. The parental A2780 cells exhibit a well-characterized genetic and epigenetic landscape, providing a relevant background for dissecting the function of DNMT3A in malignant transformation.
DNMT3A functions as a de novo DNA methyltransferase, catalyzing the transfer of a methyl group from S-adenosyl methionine to the 5′ position of cytosine in CpG dinucleotides. This activity is critical for establishing DNA methylation patterns during development and is regulated by transcription factors such as SPI1 and RUNX1, as well as post-translational modifications. DNMT3A exerts its effects by methylating promoter CpG islands of tumor suppressor genes, including CDKN2A and MLH1, leading to transcriptional repression. The enzyme interacts with regulatory partners like DNMT3L and HDAC1 and associates with histone H3 tails, coordinating epigenetic silencing at target loci. Downstream, DNMT3A drives global DNA methylation patterns that are recognized by methyl-CpG binding proteins, ultimately shaping chromatin organization and gene expression programs.
In ovarian cancer, DNMT3A dysregulation contributes to aberrant DNA hypermethylation and silencing of tumor suppressors, promoting tumorigenesis and chemoresistance. The A2780 knockout model enables precise dissection of DNMT3A’s role in ovarian cancer epigenetics. By comparing knockout and parental cells, researchers can identify DNMT3A-specific methylation targets and assess their impact on cellular phenotypes such as proliferation, invasion, and drug sensitivity. This model is particularly relevant for studying the link between DNMT3A and clonal hematopoiesis-related mutations, as well as its overlapping functions in myeloid malignancies, providing cross-cancer insights into epigenetic dysfunction.
This polyclonal knockout cell population is suitable for a range of experimental applications, including investigation of epigenetic regulation in ovarian cancer, functional studies of DNMT3A in tumorigenesis, and evaluation of sensitivity to DNA methylation inhibitors like decitabine. Researchers can perform bisulfite sequencing to profile methylation changes, Western blotting to confirm DNMT3A loss, RT-qPCR to measure target gene re-expression, and RNA-seq for transcriptome-wide analysis. Cell viability assays with hypomethylating agents further enable assessment of therapeutic vulnerabilities. These cells support epigenome editing studies and mechanistic dissection of DNMT3A-associated pathways. For additional information or technical support, please contact Ascent Research.
