ArticleNature communications2026
Targeting Prolyl 3-hydroxylase 1 inhibits pancreatic cancer progression and macrophage immunity.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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21 authors.
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Abstract
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.
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