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<p>Research on the gut microbiota has primarily focused on bacterial communities. However, the role of fungi-the second-largest eukaryotic component of the gut microbiome-in the development and progression of colorectal cancer (CRC) has been less extensively studied compared to bacteria. Recent studies have revealed significant fungal dysbiosis in the intestines of CRC patients, where the enrichment of specific pathogenic fungi (e.g., <i>Aspergillus</i> spp.) is closely associated with tumor progression, while the reduction of certain commensal fungi may weaken their protective effects. This fungal imbalance not only directly promotes tumorigenesis through carcinogenic mechanisms but also indirectly accelerates CRC progression by reshaping the bacteria-fungi interaction network and the host immune microenvironment. This article reviews the structural alterations of fungal communities in CRC, the changing patterns of specific fungal species, the relationship between fungal dysbiosis and clinicopathological features, the potential molecular mechanisms of fungi in CRC pathogenesis, the significance of cross-kingdom microbial interactions, as well as the potential diagnostic and therapeutic applications of fungi in CRC and the challenges and prospects of novel fungal-modulating therapeutic strategies.</p>

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Fungi and colorectal cancer: from dysregulation to clinical translation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月2日

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  • Wu Yinhang,
  • Han Shuwen,
  • Zhuang Jing,
  • Feng Min

摘要

Research on the gut microbiota has primarily focused on bacterial communities. However, the role of fungi-the second-largest eukaryotic component of the gut microbiome-in the development and progression of colorectal cancer (CRC) has been less extensively studied compared to bacteria. Recent studies have revealed significant fungal dysbiosis in the intestines of CRC patients, where the enrichment of specific pathogenic fungi (e.g., Aspergillus spp.) is closely associated with tumor progression, while the reduction of certain commensal fungi may weaken their protective effects. This fungal imbalance not only directly promotes tumorigenesis through carcinogenic mechanisms but also indirectly accelerates CRC progression by reshaping the bacteria-fungi interaction network and the host immune microenvironment. This article reviews the structural alterations of fungal communities in CRC, the changing patterns of specific fungal species, the relationship between fungal dysbiosis and clinicopathological features, the potential molecular mechanisms of fungi in CRC pathogenesis, the significance of cross-kingdom microbial interactions, as well as the potential diagnostic and therapeutic applications of fungi in CRC and the challenges and prospects of novel fungal-modulating therapeutic strategies.