ArticleNature communications2025
Diabetes reshapes pancreatic cancer-associated endothelial niche by accelerating senescence.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Anthropometric traits, metabolic biomarkers, and pancreatic cancer risk: a causal mediation analysis in UK Biobank.British journal of cancer · 2026Article
- Biomaterial-based strategies for postoperative residual tumors: From margin clearance to immune control and tissue repair.Materials today. Bio · 2026Review
- Spatial Multiomics Analyses Reveal That Diabetes Promotes Pancreatic Cancer Progression by Stimulating Cholesterol-Induced Neutrophil Extracellular Trap Formation.Cancer research · 2026Article
- The impact of chronic comorbidities on cancer immunoediting: challenges and opportunities for immunotherapies.Frontiers in immunology · 2026Review
- Therapy-Induced Senescence (TIS) and SASP: The p53-Mediated Interplay in Cancer Progression and Treatment.International journal of molecular sciences · 2025Review
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Authors and funding
11 authors.
Funding
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Abstract
Approximately half of pancreatic cancer patients present with comorbid diabetes. Diabetes is correlated with adverse prognostic outcomes in pancreatic cancer patients, but the underlying mechanism remains elusive. Here, we demonstrate that the cancer-associated endothelial niche is reshaped in the diabetic pancreatic tumor microenvironment and enhances the tumor-promoting capacity. Senescent endothelial cells expand in the diabetic tumor microenvironment and produce a potential senescence-associated secretory phenotype factor, i.e., INHBB. As a member of the TGF-β superfamily, INHBB promotes tumor progression and is regulated by Notch signaling. Pharmacological inhibition of INHBB receptors with bimagrumab effectively inhibited tumor progression in diabetic mice. Moreover, short-term bimagrumab treatment did not significantly decrease glucose levels in diabetic tumor-bearing mice. Combination treatment with metformin showed synergistic antitumor effects. In conclusion, our study identifies INHBB as a promising therapeutic target for pancreatic cancer with comorbid diabetes, laying the foundation for the development of individualized therapies for pancreatic cancer patients.
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