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Adrenergic nerves activate an angio-metabolic switch in prostate cancer

Ali H Zahalka1,2, Anna Arnal-Estapé1,2, Maria Maryanovich1,2

  • 1Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Science (New York, N.Y.)
|October 21, 2017
PubMed

Insights

Nerve signaling through adrenergic receptors promotes prostate cancer growth by altering blood vessel metabolism. Blocking this pathway may offer a new anticancer therapy targeting tumor angiogenesis.

Area of Science:

  • Oncology
  • Neuroscience
  • Metabolic Research

Background:

  • Nerve fibers associate with blood vessels, influencing vascular development and potentially the tumor microenvironment.
  • The precise role of nerve-derived factors in regulating tumor progression, particularly prostate cancer, remains largely undefined.

Purpose of the Study:

  • To investigate the function of endothelial adrenergic signaling in prostate cancer growth.
  • To elucidate the mechanisms by which nerve-derived signals impact tumor angiogenesis and metabolism.

Main Methods:

  • Utilized mouse models of prostate cancer to study the interaction between nerves and tumor vasculature.
  • Analyzed the role of endothelial beta-2 adrenergic receptor (Adrb2) and its signaling pathway.
  • Investigated the metabolic profiles of endothelial cells, focusing on aerobic glycolysis and oxidative phosphorylation.

Main Results:

  • Endothelial beta-2 adrenergic receptor (Adrb2) signaling, mediated by noradrenaline from prostate nerves, is crucial for activating tumor angiogenesis and growth.
  • Loss of Adrb2 in endothelial cells inhibits angiogenesis by shifting metabolism from aerobic glycolysis to enhanced oxidative phosphorylation.
  • Codeletion of Adrb2 and Cox10 rescued the metabolic changes and restored prostate cancer progression.

Conclusions:

  • Nerve-derived noradrenaline critically regulates endothelial cell metabolism and angiogenesis in prostate cancer via Adrb2.
  • Targeting the cross-talk between nerve signaling and endothelial metabolism presents a potential therapeutic strategy for prostate cancer.

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