ArticleBritish journal of cancer2026
Blockage of cuproplasia inhibits pancreatic tumour-associated neutrophils infiltration through TRAF6/STAT3/CCL2 pathway.
Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026Review
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Authors and funding
17 authors.
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Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis and is easy to developing drug resistance to conventional therapies due to its distinctive tumour microenvironment. Recent advancements have brought attention to the aberrant copper metabolism in this malignancy, but the influence of intracellular cuproplasia and balance on the tumoral immune microenvironment is still uncertain.
methodsWe analysed copper concentrations and CTR1 expression in PDAC tissues and cell lines. Spatial transcriptomics was employed to delineate the relationship between CTR1 overexpression and tumour-associated neutrophils (TANs) infiltration. Chemokine arrays and molecular assays were used to identify key signalling pathways involved. Functional experiments, including CTR1 knockdown and TRAF6 overexpression, were conducted to assess its impact on neutrophil infiltration and therapeutic synergy with gemcitabine.
resultsWe identified that CTR1 overexpression drives intracellular copper overaccumulation, activating TRAF6-dependent phosphorylation of JAK/STAT3. Phosphorylated STAT3 transcriptionally upregulates the chemokine CCL2, fostering CCR2-mediated TANs infiltration, which correlates with poor prognosis. Crucially, single-cell RNA sequencing revealed CTR1 knockdown suppresses a pro-metastatic TAN subpopulation (TAN-2) and dramatically reduces TANs recruitment in orthotopic tumour models. This copper-targeted intervention concurrently enhances cytotoxic CD8
conclusionsOur findings shed light on how intracellular copper metabolism-regulating molecules modulate the neutrophil infiltration through the TRAF6/STAT3/CCL2 pathway, and particularly, targeting the copper regulator shows potential in optimising the tumour microenvironment in the treatment of pancreatic cancers. Schematic diagram of the mechanism by which CTR1 regulates neutrophil recruitment through CCL2 transcriptional activation through the TRAF6/JAK/STAT3 Pathway.
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