ArticleMolecular cancer2025
Targeting SERPINB3-MAPK axis-mediated cuproptosis resistance enhances the response to antitumor immunotherapy.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Metabolic cell death: ferroptosis, cuproptosis, and disulfidptosis as a unified framework for targeting metabolic vulnerabilities in disease.Apoptosis : an international journal on programmed cell death · 2026Review
- LAMC2Cancer science · 2026Article
- Target FADS1-arachidonic acid-ferroptosis axis: A metabolic bridge linking matrix stiffness to PDAC stemness.Materials today. Bio · 2026Article
- Matrix stiffness induces CaExperimental hematology & oncology · 2026Article
- Cuproptosis in Sepsis: Cell Type-Specific Mechanisms and Clinical Prospects.Drug design, development and therapy · 2026Review
- Epigenetic regulation of cuproptosis in cancer: mechanisms, microenvironment, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026Review
- Rac/Cdc42 inhibitors target pancreatic cancer cells and macrophages in the tumor microenvironment.Cancer treatment and research communications · 2026Article
- Advances in Intranasal Delivery of Exosomes for Central Nervous System Disorders.Molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Cuproptosis, a newly identified form of cell death, is closely linked to copper homeostasis and protein lipoylation. Using a multi-omics approach, we firstly reveal that SERPINB3 confers cuproptosis resistance in pancreatic cancer and functions as a theranostic biomarker. Mechanistically, SERPINB3 inhibits FDX1 transcription by activating the MAPK signaling pathway, thereby conferring cuproptosis resistance. We further demonstrated that SERPINB3 directly interacts with MEK1, impeding its chaperone-mediated autophagic degradation, which ultimately leads to sustained activation of the MAPK signaling pathway. Additionally, we found that SERPINB3 promotes pancreatic cancer immune evasion by upregulating PD-L1 expression on tumor cells. This phenomenon motivated the development of a triple-combination strategy consisting of MAPK inhibition, cuproptosis induction, and αPD-1 therapy for pancreatic cancer patients with high SERPINB3 expression. To this end, we further developed a metal-organic framework (MOF) loaded with both copper ions and MEK inhibitor, which significantly triggers tumor-specific cuproptosis and enhances antitumor immunity. In summary, SERPINB3 serves as a predictive biomarker to inform therapeutic strategies targeting cuproptosis, thereby establishing a novel paradigm for cancer immunotherapy that integrates metal biology, targeted therapy, and immune modulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.