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<p>Pancreatic ductal adenocarcinoma remains one of the most formidable challenges in oncology, with limited treatment options and a poor prognosis. Understanding the key pathways affecting cancer progression is crucial for the development of therapeutic strategies. Here, we reveal a pivotal role of Prolyl 3-hydroxylase 1 in pancreatic ductal adenocarcinoma using transcriptome sequencing, proteomic analyses and engineered mouse model. Mechanistically, our findings indicate that this effect is, at least in part, through the regulation of Polo-like kinase 1 and Polo-like kinase 1-mediated β-catenin signaling. Restoration of either Prolyl 3-hydroxylase 1 or Polo-like kinase 1 expression in Prolyl 3-hydroxylase 1-deficient cells reverses the defects of β-catenin signaling, facilitates tumor cell proliferation and elicits macrophage infiltration. In addition, pharmacological inhibition of Polo-like kinase 1 strongly increases the therapeutic efficacy of chemotherapeutic response against pancreatic ductal adenocarcinoma, alleviating tumor burden in mice. Our findings suggest a promising therapeutic strategy for treating pancreatic ductal adenocarcinoma.</p>

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Targeting Prolyl 3-hydroxylase 1 inhibits pancreatic cancer progression and macrophage immunity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月13日

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  • Panzhu Bai,
  • Chengmin Liu,
  • Changying Fu,
  • Renwei Cai,
  • Yanyan Ding,
  • Meiling Quan,
  • Yuhao Ye,
  • Ziyang Zhang,
  • Yuan Li,
  • Yanfen Xu,
  • Siqi Guo,
  • Binbin Li,
  • Guizhen Li,
  • Wudi Yu,
  • Dalu Wang,
  • Ming Jiang,
  • Yi Deng,
  • Sicong He,
  • Chuanyue Wu,
  • Ruijun Tian,
  • Ying Sun

摘要

Pancreatic ductal adenocarcinoma remains one of the most formidable challenges in oncology, with limited treatment options and a poor prognosis. Understanding the key pathways affecting cancer progression is crucial for the development of therapeutic strategies. Here, we reveal a pivotal role of Prolyl 3-hydroxylase 1 in pancreatic ductal adenocarcinoma using transcriptome sequencing, proteomic analyses and engineered mouse model. Mechanistically, our findings indicate that this effect is, at least in part, through the regulation of Polo-like kinase 1 and Polo-like kinase 1-mediated β-catenin signaling. Restoration of either Prolyl 3-hydroxylase 1 or Polo-like kinase 1 expression in Prolyl 3-hydroxylase 1-deficient cells reverses the defects of β-catenin signaling, facilitates tumor cell proliferation and elicits macrophage infiltration. In addition, pharmacological inhibition of Polo-like kinase 1 strongly increases the therapeutic efficacy of chemotherapeutic response against pancreatic ductal adenocarcinoma, alleviating tumor burden in mice. Our findings suggest a promising therapeutic strategy for treating pancreatic ductal adenocarcinoma.