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<p>Hepatocellular carcinoma (HCC) remains a major global health challenge due to its aggressive nature and limited treatment options. This review aims to clarify the oncogenic role of FOXM1 in HCC and its potential as a therapeutic target. We examine how FOXM1 drives cancer development by regulating key cellular processes such as cell cycle progression, proliferation, metastasis, and therapy resistance. The review details mechanisms that control FOXM1 activity, including transcriptional regulation by upstream factors, post-transcriptional modulation via non-coding RNAs, and epigenetic modifications. We also explore how FOXM1 interacts with critical signaling pathways, such as AKT, p53, ERK, Hedgehog, STAT3, and Wnt/β-catenin, to promote metabolic reprogramming, angiogenesis, and the maintenance of cancer stem cell properties. In the therapeutic section, we assess emerging strategies that target FOXM1, including small-molecule inhibitors, proteasome inhibitors, and immunotherapeutic approaches, to improve treatment outcomes for HCC patients. This comprehensive review highlights the pivotal role of FOXM1 in HCC pathogenesis and provides novel avenues for targeted intervention.</p>

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The oncogenic role of FOXM1 in hepatocellular carcinoma: molecular mechanisms, clinical significance, and therapeutic potentials

  • 期刊论文

  • 发表日期：

    2025年4月23日

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  • Fangyu He,
  • He Liu,
  • Fangcheng Zhao

摘要

Hepatocellular carcinoma (HCC) remains a major global health challenge due to its aggressive nature and limited treatment options. This review aims to clarify the oncogenic role of FOXM1 in HCC and its potential as a therapeutic target. We examine how FOXM1 drives cancer development by regulating key cellular processes such as cell cycle progression, proliferation, metastasis, and therapy resistance. The review details mechanisms that control FOXM1 activity, including transcriptional regulation by upstream factors, post-transcriptional modulation via non-coding RNAs, and epigenetic modifications. We also explore how FOXM1 interacts with critical signaling pathways, such as AKT, p53, ERK, Hedgehog, STAT3, and Wnt/β-catenin, to promote metabolic reprogramming, angiogenesis, and the maintenance of cancer stem cell properties. In the therapeutic section, we assess emerging strategies that target FOXM1, including small-molecule inhibitors, proteasome inhibitors, and immunotherapeutic approaches, to improve treatment outcomes for HCC patients. This comprehensive review highlights the pivotal role of FOXM1 in HCC pathogenesis and provides novel avenues for targeted intervention.