ArticlePeerJ2025
The 12-LOX/12-HETE/GPR31 metabolic pathway promotes tumor-associated macrophage M2 polarization mediated pancreatic cancer development.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Association of ALOX12-Mediated AA/12-HETE Metabolic Dysregulation with Abdominal Aortic Aneurysm Enlargement and Dissection.Journal of cardiovascular development and disease · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The 12-lipoxygenase (12-LOX)/12-hydroxyeicosatetraenoic acid (12-HETE) pathway is associated with various tumors. M2 macrophages in the tumor microenvironment promote tumorigenesis and progression. However, the role of the 12-LOX/12-HETE/G protein-coupled receptor 31 (GPR31) metabolic pathway and its relationship with M2 macrophages remains unclear in pancreatic cancer (PC). Methods: The expression levels of 12-LOX, GPR31, and 12-HETE were detected in PC and mouse PC models using western blot and enzyme-linked immunosorbent assays (ELISA). Results: The 12-LOX/12-HETE/GPR31 metabolic pathway is expressed actively in PC. Inhibition of 12-LOX in a mouse model of pancreatic cancer suppressed the expression of this metabolic pathway, retarded tumor growth, and reduced the polarization of macrophages towards the M2 type. Conclusion: This study, through
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