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. 2023 Jan 10;30:3. doi: 10.1186/s12929-022-00893-0

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© The Author(s) 2023

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. 4 — Therapeutic effects of DNMT inhibitors on different types of immune cells in the tumor immune microenvironment. DNA methyltransferase inhibitors (DNMTis) possess both anti-tumor and pro-tumor effects via reprogramming different immune cell types in TIME. DNMTi treatment of cancer cells exerts anti-tumor memory effects, induces anti-viral interferon responses, promote expression of tumor-associated antigens, as well as upregulation of antigen processing and presentation machineries, which enhances the recognition and lysis of cancer cells by effector T cells. Besides, DNMTi appears to reinvigorate dysfunctional T cells and shift the exhaustion state towards an effector T cell phenotype. Furthermore, DNMTi significantly promotes immune synapse formation and cytoskeletal reorganization, leading to robust cancer killing by cytotoxic γδ T cells. Besides, DNMTi promotes anti-tumor immunity by reducing myeloid-derived suppressor cells (MDSC) and disrupting premetastatic niches established by MDSC. Interestingly, DNMTis show bifacial effects on natural killer (NK) cells and may either suppress NK cell-mediated cancer killing or boost NK cell-mediated recognition of cancer cells. On the other hand, DNMTi may exert pro-tumor effects by promoting lineage development and suppressive function of Treg. This figure was created on BioRender.com