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. 2020 Sep 29;8:49. doi: 10.1186/s40364-020-00228-x

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© The Author(s) 2020

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Mechanisms of interferon-γ mediated cancer regression. The IFN-γ stimulates activation of JAK/STAT signaling in the TME what further drives increased caspase activity and downregulation of SLC7A11 and SLC3A2. Consequently, cancer cells undergone apoptosis directly or through induced lipid peroxidation and ferroptosis. IFN-γ induces fragility of Tregs and inhibits the formation of tumor blood vessels by downregulating VEGF-A. Additionally, tumor angiogenesis is inhibited by IFN-γ-induced endothelial cells destruction. Through stimulation of M1 macrophage polarization and inhibition of their M2 phenotype, it contributes to effective antitumor immune response. The IFN-γ can stimulate p16INK4a-Rb pathway and thus, tumor senescence, while IFN-γ-mediated activation of IDO1-Kyn-AhR-p27 pathway shifts tumors to a dormant state. Moreover, IFN-γ increases FN1 expression that limits cancer metastasis. SLC7A11-solute carrier family 7 member 11; SLC3A2-solute carrier family 3 member 2); IDO1-indoleamine 2,3-dioxygenase 1; Kyn-kynurenine; AhR-aryl hydrocarbon receptor; p27-cyclin-dependent kinase inhibitor 1B; p16INK4a-p16(INK4a) cyclin-dependent kinase; Rb-retinoblastoma; FN1-fibronectin-1