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. 2023 Mar 1;42(13):941–951. doi: 10.1038/s41388-023-02640-7

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — A Transcription. ecDNA can transcribing into RNAs for protein translation or regulating gene expression. B Detection maker. Tumor cells release ecDNA into the blood circulation and thus serve as a tumor detection marker. C Copy-number amplification. Unequal division of ecDNA leads to rapid amplification of oncogenes carried on ecDNA compared to chromosomal DNA. D Intratumoral heterogeneity. Random assignment during ecDNA replication leads to tumor heterogeneity. E Drug resistance. Continuous amplification of ecDNA containing resistance genes leads to drug resistance in tumor cells. F Reshaping cancer genome. If ecDNA is integrated into the upstream of the proto-oncogene, it can enhance the expression of the proto-oncogene, and if integrated into the tumor suppressor gene, it will cause loss of tumor suppressor gene function. G Regulatory circuitry on ecDNA. Multiple ecDNA aggregates to form ecDNA hubs, the enhancers and promoters carried on ecDNA act on protein-coding genes, facilitating the transcription of oncogenes.