Extrachromosomal DNA as a Non-Coding RNA Production Platform: Three Mechanistic Hypotheses for ecDNA-Driven Immune Evasion, Chromatin Remodeling, and Metastatic Colonization in Colorectal Cancer
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Extrachromosomal DNA (ecDNA) has emerged as a critical oncogenic alteration in colorectal cancer (CRC) and other aggressive malignancies, characterized by its open chromatin configuration, transcriptional hyperactivity, and ability to form nuclear condensate hubs with trans-regulatory functions. While the protein-coding oncogene amplification function of ecDNA is well-established, its role as a production platform for non-coding RNAs (ncRNAs) — including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) — remains essentially unstudied. Here we present three mechanistic hypotheses connecting ecDNA biology to ncRNA-mediated regulatory programs in CRC:
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