The DNMT3A Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt DNMT3A expression in a human hepatic adenocarcinoma background. This product provides a genetically modified pool of SK-HEP-1 cells with disrupted DNMT3A, serving as a loss-of-function model for studying de novo DNA methylation and epigenetic regulation in liver cancer.
SK-HEP-1 is a human hepatic adenocarcinoma cell line derived from ascites, exhibiting adherent epithelial morphology. It is widely used as a model for hepatocellular carcinoma (HCC) and liver cancer biology, enabling investigation of oncogenic mechanisms, tumor progression, and therapeutic responses in a hepatic context.
DNMT3A is a de novo DNA methyltransferase that catalyzes the transfer of methyl groups to CpG dinucleotides, leading to transcriptional silencing. It is regulated by upstream factors such as SP1, NF-??B, Wnt signaling, and E2F1, and it targets promoters of tumor suppressor genes like CDKN2A and RASSF1A for methylation, thereby repressing their transcription. Additionally, DNMT3A silences pluripotency genes OCT4 and NANOG. It interacts with cofactors including DNMT3L, HDAC1, UHRF1, PCNA, and SIN3A to form repressive complexes that coordinate methylation with chromatin remodeling. Together with DNMT1, DNMT3B, and UHRF1, DNMT3A is a central component of the DNA methylation machinery, mediating epigenetic modifications essential for development and disease.
In SK-HEP-1 cells, DNMT3A knockout provides a powerful tool to dissect the role of aberrant DNA methylation in hepatocellular carcinoma. Since DNMT3A is implicated in silencing tumor suppressors in liver cancer, its disruption allows researchers to investigate the reactivation of silenced genes and the consequences on cell proliferation, apoptosis, migration, and drug sensitivity. This model is particularly relevant for studying epigenetic mechanisms driving HCC progression and for evaluating DNMT3A as a therapeutic target.
This polyclonal knockout cell population is suitable for a wide range of assays, including western blotting and RT-qPCR to confirm loss of DNMT3A expression, bisulfite sequencing to assess global or locus-specific DNA methylation changes, ChIP-seq to map DNA methylation patterns, and RNA-seq to analyze transcriptomic alterations. Functional studies can employ apoptosis and migration/invasion assays, and drug sensitivity screening to identify compounds that interact with epigenetic pathways. This model supports research into cancer epigenetics, drug development, and the molecular underpinnings of liver cancer. For additional information, please contact Ascent Research.
