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  • The stress-microbiome-cancer triad and the impact of catecholamines on Host-Microbe Interactions and tumor progression

  • Narjes Sangin ,1,*
    1. Department of Cell and Molecular Biology, Faculty of Chemistry, University of Kashan, Kashan, Iran


  • Introduction: Two types of psychological stress exist: acute and chronic. The fight or flight response is influenced by stress that lasts from a few minutes to several hours and can persist for weeks, months, and years. Substances, chemicals, and biological agents are all exogenous factors. Chronic stress is the fourth most common cause of cancer. While catecholamine secretion is adaptive during acute stress conditions, it causes a sustained surge in circulating norepinephrine and epinépherine in chronic stress states, which may lead to metabolic disorders and cancer. Through the release of hormones like cortisol, adrenaline, and noradrenaline to regulate stress, alter the microbial species' abundance or composition, improve intestinal permeability in large quantities, trigger inflammatory responses, leading to psychological symptoms such as anxiety and depression. Chronic stress causes depression that promotes the growth of tumor tissue through aerobic glycolysis, which is essential for fueling their growth. This cycle is not a one-way process, and the tumor's secretion of inflammatory substances leads to an unidirectional depression that promotes cancer progression.
  • Methods: By triggering chronic stress hormones, the body impaird the ability of NK cells and killer T cells to differentiate from and eliminate cancer cells, while activating immunosuppressive cells that produce tumor-causing proteins and melanocytes. The NF-KB signaling pathway and inflammatory factors such as IL-6, il-8, and TNFalpha experience a sustained surge due to chronic stress. Stress-induced activation of the sympathetic nervous system leads to the proliferation of tumors through proinflammatory cytokines like MMP-9 and MSP-2. Norepinephrine is believed to trigger signaling pathways such as MAPK, ERK, MEK and AKT by binding to alpha- and beta-adrenergic receptors on cancer cells, leading to proliferation, migration and invasion of cancer cell lines according to a 2025 study.
  • Results: Certain digestive tract-eating microorganisms generate a group of metabolites that may confer tumorigenic properties or inhibit tumor growth. We conclude that the link between cancer and the gut microbiome is not solely dependent on tumors, as even cancer treatments can disrupt the intestinal microbe's balance.
  • Conclusion: Brain cancer is a complex illness that arises from the interplay between the gut microbiome and the nervous system, which are linked to the so-called gut-brain axis of cancer. Small amounts of short-chain fatty acids (SCFAs), tryptophan-derived compounds, secondary bile acids, lipopolysaccharides, and other metabolic substances are produced by gut microorganisms and can play a crucial role in immune response regulation as well as neuroinflammation and tumorigenesis. Moreover, these substances can influence immune responses, the blood-brain barrier integrity, and the microenvironment surrounding a tumor.' Moreover, studies have revealed that high-fiber and fermentable diets, along with fecal transplantation and probiotics can improve the immune system, decrease inflammation, and boost therapeutic efficacy. PropranoloL and metoprolidon, which are beta-blockers, have been suggested as potential therapeutic options. These beta-blockers inhibit the activity of beta receptors and regulate tumor growth by blocking glycolysis and oxidative phosphorylation pathways in tumor cells, which boosts CD28 expression and antitumor functions.
  • Keywords: Catecholamines, Microbiome, Chronic Stress, inflammation, Tumor Progression

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