ArticleCancer immunology, immunotherapy : CII2025
Chronic stress promotes pancreatic ductal adenocarcinoma progression via complement C5a-recruited myeloid-derived suppressor cells.
Article in Cancer immunology, immunotherapy : CII, 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.
- Neuron-tumor crosstalk in cancer: molecular mechanisms and translational advances.Molecular cancer · 2026Review
- Humoral immunity in pancreatic cancer: B-cell heterogeneity, regulatory networks, and therapeutic opportunities.Cancer metastasis reviews · 2026Review
- Myeloid-derived suppressor cells in colorectal cancer: mechanisms of immunosuppression, therapy resistance and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- A hypothesis and evidence map for neuroimmune regulation of DOCK-family cytoskeletal programs in solid tumors.Frontiers in immunology · 2026Review
- EUS-guided neurolysis as a translational approach to tumor-promoting innervation in pancreatic cancer.Endoscopic ultrasoundArticle
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Authors and funding
16 authors.
Funding
Abstract
Chronic stress is an established risk factor for pancreatic ductal adenocarcinoma (PDAC). Although the autonomic nervous system (ANS), a key component of the tumor microenvironment (TME), has been closely associated with PDAC pathogenesis and prognosis, the underlying mechanisms remain incompletely understood. This study reveals that chronic stress-induced sympathetic nervous system (SNS) activation upregulates the hepatic complement system, leading to the recruitment of myeloid-derived suppressor cells (MDSCs) that promotes tumor progression. Specifically, chronic stress-triggered neurotransmitter norepinephrine (NE) enters the liver via systemic circulation and binds to upregulated β1 adrenergic receptor (ADRB1) on hepatocytes, enhancing the expression of complement components C3, C5, and CFH. In murine chronic stress-model, elevated systemic and intratumoral complement component 5a (C5a) levels correlated positively with MDSC expansion in both the spleen and tumor tissues. The effect was abrogated by the C5aR1 antagonist PMX-53, identifying C5a as a critical mediator of MDSC accumulation. MDSCs infiltrating the TME exhibited elevated expression of programmed death-ligand 1 (PD-L1) and transforming growth factor-β (TGF-β), contributing to an immunosuppressive niche. Intervention with the ADRB1 antagonist atenolol in PDAC mice significantly reduced serum/tumoral C5a levels, diminished splenic/intratumoral MDSCs proportions, and attenuated tumor growth. Our findings propose that targeting the SNS-driven complement-MDSCs axis represents a promising strategy for PDAC patients.
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