ArticleInternational journal of molecular sciences2025
Identification and Characterization of eccDNA in HepG2 Cells Under DOX-Induced DNA Damage.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Deciphering the role of cell-free extrachromosomal circular DNA in human heart failure.Human genomics · 2026Article
- Stimuli-Responsive Calcium Phosphate Nanoreactor for Synergistic Chemo-Photothermal-Ferroptosis Therapy of Colorectal Cancer.International journal of nanomedicine · 2026Article
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9 authors.
Funding
Abstract
Extrachromosomal circular DNA (eccDNA) has been recognized as a key player in tumorigenesis and progression. However, eccDNA transcriptional regulatory mechanisms under DNA damage in cancer remain poorly characterized. Here, we used doxorubicin to induce DNA damage in the hepatocellular carcinoma cell line HepG2 and performed Circle-seq to profile eccDNAs before and after the damage. We observed a significant increase in the number, length, and chromosomal distribution density of eccDNAs following DNA damage. RNA-seq revealed that the expression of genes carried on eccDNA was positively correlated with eccDNA copy number under DNA damage. Further ATAC-seq profiling identified distinct chromatin characteristics at eccDNA breakpoint regions compared to other regions of eccDNA and linear genomic regions. Additionally, eccDNAs generated under DNA damage preferentially originated from linear genomic regions characterized by low GC content and hypomethylation. Finally, by integrating Hi-C and H3K27ac ChIP-seq, we uncovered that eccDNAs with mobile enhancer activity (ME-eccDNAs) display significantly enhanced chromatin interactions and H3K27ac enrichment after DNA damage. Overall, our findings systematically elucidate the DNA damage-driven mechanisms underlying eccDNA biogenesis, chromatin characteristics and transcriptional regulation in HCC HepG2 cells.
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