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. 2022 Jun 1;24(10):1337–1349. doi: 10.1007/s11912-022-01295-z

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© The Author(s) 2022

Open AccessThis 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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Fig. 1 — Antagonists of mu-opioid receptor biochemical mechanisms of antineoplastic action. A: Low-dose naltrexone biochemical mechanisms of antineoplastic action. B: Methylnaltrexone biochemical mechanisms of antineoplastic action. OGF: opioid growth factor; OGFr: opioid growth factor receptor; KOR: κ opioid receptor; DOR: δ opioid receptor; MOR: µ opioid receptor; BMDCs: bone marrow-derived dendritic cells; S1PR3: sphingosine-1-phosphate receptor 3; mTOR: mammalian target of rapamycin; : inhibitory effect

Inline graphic — Antagonists of mu-opioid receptor biochemical mechanisms of antineoplastic action. A: Low-dose naltrexone biochemical mechanisms of antineoplastic action. B: Methylnaltrexone biochemical mechanisms of antineoplastic action. OGF: opioid growth factor; OGFr: opioid growth factor receptor; KOR: κ opioid receptor; DOR: δ opioid receptor; MOR: µ opioid receptor; BMDCs: bone marrow-derived dendritic cells; S1PR3: sphingosine-1-phosphate receptor 3; mTOR: mammalian target of rapamycin; : inhibitory effect