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<p>Over the past decade, increasing evidence has linked the dysregulation of human protein <i>O</i>-fucosyltransferase 1 (POFUT1), overwhelmingly through gene overexpression, to tumor progression in multiple cancers, including colorectal, breast, gastric, lung, hepatocellular carcinoma, and glioblastoma. This review provides a comprehensive analysis of the molecular and cellular consequences of POFUT1 dysfunction in cancer. <i>POFUT1</i> overexpression driven by copy number variations (CNVs), epigenetic alterations, and/or post-transcriptional modifications enhances tumorigenesis by activating key oncogenic pathways such as Notch, Wingless-type MMTV integration site family (Wnt)/β-catenin, and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR). These pathways promote cell proliferation, migration, and epithelial-mesenchymal transition (EMT) while simultaneously suppressing apoptosis. Additionally, POFUT1 promotes an immunosuppressive tumor microenvironment that contributes to treatment resistance by immune checkpoint inhibitors. Mainly, its overexpression is detectable at early stages of tumor development and in some cancer patient sera, highlighting its potential as a non-invasive biomarker for early cancer detection and disease monitoring. Given its role in immune evasion and therapy resistance, POFUT1 represents a promising therapeutic target, warranting further investigation into its clinical applications.</p>

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POFUT1 as a cancer biomarker: insights into its oncogenic mechanisms and clinical relevance

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月7日

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  • Oumaima Mazour,
  • Sébastien Legardinier,
  • Bouabid Badaoui,
  • Agnès Germot

摘要

Over the past decade, increasing evidence has linked the dysregulation of human protein O-fucosyltransferase 1 (POFUT1), overwhelmingly through gene overexpression, to tumor progression in multiple cancers, including colorectal, breast, gastric, lung, hepatocellular carcinoma, and glioblastoma. This review provides a comprehensive analysis of the molecular and cellular consequences of POFUT1 dysfunction in cancer. POFUT1 overexpression driven by copy number variations (CNVs), epigenetic alterations, and/or post-transcriptional modifications enhances tumorigenesis by activating key oncogenic pathways such as Notch, Wingless-type MMTV integration site family (Wnt)/β-catenin, and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR). These pathways promote cell proliferation, migration, and epithelial-mesenchymal transition (EMT) while simultaneously suppressing apoptosis. Additionally, POFUT1 promotes an immunosuppressive tumor microenvironment that contributes to treatment resistance by immune checkpoint inhibitors. Mainly, its overexpression is detectable at early stages of tumor development and in some cancer patient sera, highlighting its potential as a non-invasive biomarker for early cancer detection and disease monitoring. Given its role in immune evasion and therapy resistance, POFUT1 represents a promising therapeutic target, warranting further investigation into its clinical applications.