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Dear Colleagues,

Recently, a growing number of studies have suggested that bio-behavioral factors, especially various stress-related persistent stimulations, might accelerate cancer progression, which is mainly due to β-adrenergic system activation.

β-Adrenergic receptors on the tumor and stromal cells are activated by catecholamines such as adrenaline and noradrenaline. Based largely on retrospective analyses, pharmacological inhibition of the β-adrenergic receptors using beta blockers has shown clinical anticancer efficacy in many human cancers. In particular, recent advances have evidenced a role of the β3-adrenoreceptor in different pathways involved in cancer progression, apoptosis, antioxidant action, metastasis, and microenvironmental transformation.

This Special Issue on “Pleiotropic effect of β-Adrenergic receptors in human cancers” of the International Journal of Molecular Sciences aims at providing new insights into the various functions of β-Adrenergic receptors in the several aspects of cancer progression mechanisms.

Dr. Claudio Favre
Guest Editor

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Keywords

tumor microenvironment
β3-adrenoreceptor
β2-adrenoreceptor
metastasis
antioxidant activity
cancer

Published Papers (2 papers)

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Research

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16 pages, 1266 KiB

Open AccessArticle

β-Adrenoceptor Activation in Breast MCF-10A Cells Induces a Pattern of Catecholamine Production Similar to that of Tumorigenic MCF-7 Cells

by Filipa Amaro, Dany Silva, Henrique Reguengo, José C. Oliveira, Clara Quintas, Nuno Vale, Jorge Gonçalves and Paula Fresco

Int. J. Mol. Sci. 2020, 21(21), 7968; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217968 - 27 Oct 2020

Cited by 18 | Viewed by 2881

Abstract

Adrenaline, which participates in the neuroendocrine response that occurs during stress and perimenopause, may be tumorigenic. This exploratory study aimed at investigating whether non-tumorigenic and tumorigenic human breast epithelial cell lines are able to synthesize adrenaline. The study was carried out in non-tumorigenic (MCF-10A) and tumorigenic (MCF-7) human breast cell lines. Expression of enzymes involved in adrenaline synthesis was characterized by RT-qPCR, immunocytochemistry and western blot. Catecholamines and analogue compounds were quantified by HPLC-ECD. Functional assessment of the impact of drugs on cells’ tumorigenic potential was assessed by determination of cell viability and clonogenic ability. Both MCF-10A and MCF-7 cells produce catecholamines, but the capacity to produce adrenaline is lower in MCF-10A cells. β-adrenoceptor activation increases the capacity of MCF-10A cells to produce adrenaline and favor both cell viability and colony formation. It is concluded that exposure of human breast epithelial cells to β-adrenoceptor agonists increases cell proliferation and the capacity to produce adrenaline, creating an autocrine potential to spread these adrenergic effects in a feed-forward loop. It is conceivable that these effects are related to tumorigenesis, bringing a new perspective to understand the claimed anticancer effects of propranolol and the increase in breast cancer incidence caused by stress or during perimenopause. Full article

(This article belongs to the Special Issue Pleiotropic Effect of β-Adrenergic Receptors in Human Cancers and Other Human Disease)

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Review

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12 pages, 735 KiB

Open AccessReview

β3-Adrenoreceptors as ROS Balancer in Hematopoietic Stem Cell Transplantation

by Amada Pasha, Maura Calvani and Claudio Favre

Int. J. Mol. Sci. 2021, 22(6), 2835; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22062835 - 11 Mar 2021

Cited by 7 | Viewed by 3627

Abstract

In the last decades, the therapeutic potential of hematopoietic stem cell transplantation (HSCT) has acquired a primary role in the management of a broad spectrum of diseases including cancer, hematologic conditions, immune system dysregulations, and inborn errors of metabolism. The different types of HSCT, autologous and allogeneic, include risks of severe complications including acute and chronic graft-versus-host disease (GvHD) complications, hepatic veno-occlusive disease, lung injury, and infections. Despite being a dangerous procedure, it improved patient survival. Hence, its use was extended to treat autoimmune diseases, metabolic disorders, malignant infantile disorders, and hereditary skeletal dysplasia. HSCT is performed to restore or treat various congenital conditions in which immunologic functions are compromised, for instance, by chemo- and radiotherapy, and involves the administration of hematopoietic stem cells (HSCs) in patients with depleted or dysfunctional bone marrow (BM). Since HSCs biology is tightly regulated by oxidative stress (OS), the control of reactive oxygen species (ROS) levels is important to maintain their self-renewal capacity. In quiescent HSCs, low ROS levels are essential for stemness maintenance; however, physiological ROS levels promote HSC proliferation and differentiation. High ROS levels are mainly involved in short-term repopulation, whereas low ROS levels are associated with long-term repopulating ability. In this review, we aim summarize the current state of knowledge about the role of β3-adrenoreceptors (β3-ARs) in regulating HSCs redox homeostasis. β3-ARs play a major role in regulating stromal cell differentiation, and the antagonist SR59230A promotes differentiation of different progenitor cells in hematopoietic tumors, suggesting that β3-ARs agonism and antagonism could be exploited for clinical benefit. Full article

(This article belongs to the Special Issue Pleiotropic Effect of β-Adrenergic Receptors in Human Cancers and Other Human Disease)

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