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Epitranscriptomic regulation in cholangiocarcinoma: mechanisms and therapeutic implications
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DOI：10.1186/s12967-026-08740-8.png)
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Abstract
En 中文
Cholangiocarcinoma (CCA) is the second most common primary liver cancer. It is highly invasive, shows early metastasis, and frequently recurs after surgery. These features result in poor clinical outcomes and limited treatment options. Increasing evidence indicates that epigenetic dysregulation plays a key role in the initiation and progression of CCA. Epigenetic modifications include covalent changes to DNA, RNA, and histone proteins. These modifications regulate chromatin structure and gene expression, thereby shaping malignant cellular behavior. Recent studies have shown that epigenetic regulatory networks are widely disrupted in CCA. This disruption leads to both transcriptional and post-transcriptional reprogramming, which promotes tumor growth, invasion, and therapeutic resistance. Among these mechanisms, epitranscriptomic regulation has emerged as an important layer of gene expression control. RNA modifications, such as m6A and other chemical marks, influence RNA stability, splicing, translation, and degradation. These processes contribute to tumor initiation and progression. In this review, we summarize recent advances in epitranscriptomic regulation in CCA. We highlight key regulatory mechanisms and their functional roles in tumor biology. A better understanding of these pathways may provide new biomarkers and therapeutic targets for CCA.
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