β2 Adrenergic-Neurotrophin Feedforward Loop Promotes Pancreatic Cancer
Open accessAbstract
Catecholamines stimulate epithelial proliferation, but the role of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Catecholamines promoted ADRB2-dependent PDAC development, nerve growth factor (NGF) secretion, and pancreatic nerve density. Pancreatic Ngf overexpression accelerated tumor development in LSL-Kras+/G12D;Pdx1-Cre (KC) mice. ADRB2 blockade together with gemcitabine reduced NGF expression and nerve density, and increased survival of LSL-Kras+/G12D;LSL-Trp53+/R172H;Pdx1-Cre (KPC) mice. Therapy with a Trk inhibitor together with gemcitabine also increased survival of KPC mice. Analysis of PDAC patient cohorts revealed a correlation between brain-derived neurotrophic factor (BDNF) expression, nerve density, and increased survival of patients on nonselective β-blockers. These findings suggest that catecholamines drive a feedforward loop, whereby upregulation of neurotrophins increases sympathetic innervation and local norepinephrine accumulation.
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Renz et al. demonstrated in a cohort of 631 PDAC patients that intake of a non-selective betablocker, such as propranolol, led to improved overall survival compared to patients without betablocker therapy (40 vs 23 months median overall survival).
“Furthermore, they demonstrated in a cohort of 631 PDAC patients that the intake of a non-selective betablocker, such as propranolol, led to an improved overall survival compared to patients without betablocker therapy (40 vs. 23 months median overall survival) [25].”
From Pancreatic resection with perioperative drug repurposing of propranolol and etodolac – the phase II randomized controlled PROSPER trial (2025) · cites this paper as [25]
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Experimental — accuracy not yet measuredThe tumor-promoting effect of catecholamines is mainly mediated by the β2 adrenergic receptor activating the cAMP-PKA signaling pathway, which enhances tumor angiogenesis and promotes growth of malignant cells.
“The tumor-promoting effect of catecholamines is mainly mediated by the β2 adrenergic receptor (encoded by ADRB2) activating the cAMP-protein kinase A (PKA) signaling pathway, which is the main mechanism to enhance tumor angiogenesis in the body and promote the growth of malignant cells [(34, 35); Figure 2].”
From Chronic Stress Promotes Cancer Development (2020) · cites this paper as [35]
The Results (page unavailable) link ADRB2 and PKA signaling to increased pancreatic cancer cell growth and neurotrophin secretion. The Discussion (page unavailable) describes a feed-forward mechanism involving nerve growth and tumor growth, not angiogenesis. The copy does not establish angiogenesis as the main mechanism or extend this finding to malignant cells generally. (LLM, conf=0.88)
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- Authors
- Renz, B. W., Takahashi, R., Tanaka, T., Macchini, M., Hayakawa, Y., Dantes, Z., Maurer, H. C., Chen, X., Jiang, Z., Westphalen, C. B., Ilmer, M., Valenti, G., Mohanta, S. K., Habenicht, A. J. R., Middelhoff, M., Chu, T., Nagar, K., Tailor, Y., Casadei, R., Di Marco, M., Kleespies, A., Friedman, R. A., Remotti, H., Reichert, M., Worthley, D. L., Neumann, J., Werner, J., Iuga, A. C., Olive, K. P., & Wang, T. C.
- Affiliations
- Columbia University Irving Medical Center (US)
- TUM Klinikum (DE)
- Ludwig-Maximilians-Universität München (DE)
- Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten (DE)
- IRCCS Azienda Ospedliero-Universitaria di Bologna Policlinico di Sant'Orsola (IT)
- Corresponding author
- Wang, Timothy C.
- ORCID
- Renz, Bernhard W.
- Takahashi, Ryota
- Macchini, Marina
- Hayakawa, Yoku
- Dantes, Zahra
- Maurer, H. Carlo
- Chen, Xiaowei
- Jiang, Zhengyu
- Westphalen, C. Benedikt
- Ilmer, Matthias
- Mohanta, Sarajo K.
- Habenicht, Andreas J.R.
- Middelhoff, Moritz
- Chu, Timothy
- Nagar, Karan
- Casadei, Riccardo
- Friedman, Richard A.
- Remotti, Helen
- Reichert, Maximilian
- Worthley, Daniel L.
- Neumann, Jens
- Werner, Jens
- Iuga, Alina C.
- Olive, Kenneth P.
- Wang, Timothy C.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 33
- Issue
- 1
- Pages
- 75-90.e7
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC5760435
- OpenAlex
- W2771271491
- Cited by
- 543
- References
- 9
- Citations by year
- 2026: 93 · 2025: 87 · 2024: 70 · 2023: 68 · 2022: 62 · 2021: 66 · 2020: 50 · 2019: 32 · 2018: 13 · 2017: 1
- FWCI
- 21.57
- Type
- journal article
- Language
- en
- Update notices
- erratum (2018-11-12)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, cc-by-nc-nd)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Funders
- NIH (P30CA013696, S10RR025686, R35CA210088)
- Cancer Center Flow Core Facility (P30CA013696)
- Plexxikon Inc.
- Pancreatic Cancer Action Network - ACCR
- Lustgarten Foundation
- German Research Foundation (DFG RE3440/1-1, DFG MO3054/1-1, DFG HA1083/15-4)
- Uehara Memorial Foundation
- Japanese Society of Gastroenterology
- Japan Agency of Medical Research and Development
- National Pancreas Foundation
- German Cancer Aid Foundation
- KKF Program
- AGA-Actavis Research Award
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- pancreatic ductal adenocarcinoma, beta2-adrenergic receptor, catecholamines, sympathetic innervation, nerve growth factor, brain-derived neurotrophic factor, norepinephrine, feed-forward loop, KPC mice, gemcitabine, beta-blockers, tumor progression, patient survival
- MeSH terms
- Gemcitabine, Animals, Carcinoma in Situ, Catecholamines, Deoxycytidine, Mice, Transgenic, Nerve Growth Factors, Pancreatic Neoplasms, Adrenergic Agents, Cell Line, Tumor
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