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. 2022 Sep 8;12:15058. doi: 10.1038/s41598-022-18324-3

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Potential antitumor activity and therapeutic benefits of repurposed β-blocker propranolol in osteosarcoma. β-AR signaling is involved in cancer progression and is upregulated in osteosarcoma (OSA). Its activation by catecholamines in tumor cells, as well as in other stromal players such as vascular and immune cells (i.e. neutrophils, macrophages, T cells, among others), promotes cell growth and angiogenesis, favors the formation of immune permissive niches and accelerates tumor progression. Besides antagonizing the growth-stimulating effects of catecholamines, treatment of ADRB2-expressing OSA cells with β-blocker propranolol (PPN) seems to inhibit cellular growth and chemotaxis by blocking cell cycle progression and altering actin cytoskeleton dynamics. PPN treatment could complement chemotherapy by inhibiting OSA-induced angiogenesis, enhancing tumor necrosis and thus delaying disease progression. With the aim of advancing PPN repurposing towards clinical practice further studies regarding its anti-OSA mechanisms of action are warranted, including its potential impact on tumor immune microenvironment and metastatic spread.