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<p>Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with a poor prognosis, underscoring the urgent need to identify novel therapeutic targets. The epigenetic regulator TET1, a key enzyme involved in active DNA demethylation, has been implicated in various cancers, however, its precise role in HCC remains controversial and poorly defined. This study demonstrates that TET1 is significantly upregulated in HCC tissues, and elevated TET1 expression is associated with advanced tumor stage, shorter overall survival and reduced disease-free survival in patients. Functional assays revealed that TET1 knockdown significantly suppressed HCC cell proliferation and induced apoptosis; it also triggered G1-phase cell cycle arrest. Mechanistically, we found that the oncogenic effects of TET1 are mediated through activation of the PI3K/Akt signaling pathway. In summary, our results establish TET1 as a critical promoter of HCC progression and elucidate its role in regulating the PI3K/Akt pathway. These findings highlight its value as both a prognostic biomarker and a potential therapeutic target in HCC.</p>

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TET1 suppresses hepatocellular carcinoma progression by modulating the PI3K/Akt signaling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Shuaiyong Qi,
  • Ming Chen,
  • Zhixian Ding,
  • Mike Dai,
  • Lusheng Wang,
  • Jie Chen,
  • Yu Tang,
  • Mengxue Hu,
  • Yafei Li,
  • Kemeng Tan,
  • Lili Li,
  • Hui Jiang,
  • Heng Tang

摘要

Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with a poor prognosis, underscoring the urgent need to identify novel therapeutic targets. The epigenetic regulator TET1, a key enzyme involved in active DNA demethylation, has been implicated in various cancers, however, its precise role in HCC remains controversial and poorly defined. This study demonstrates that TET1 is significantly upregulated in HCC tissues, and elevated TET1 expression is associated with advanced tumor stage, shorter overall survival and reduced disease-free survival in patients. Functional assays revealed that TET1 knockdown significantly suppressed HCC cell proliferation and induced apoptosis; it also triggered G1-phase cell cycle arrest. Mechanistically, we found that the oncogenic effects of TET1 are mediated through activation of the PI3K/Akt signaling pathway. In summary, our results establish TET1 as a critical promoter of HCC progression and elucidate its role in regulating the PI3K/Akt pathway. These findings highlight its value as both a prognostic biomarker and a potential therapeutic target in HCC.