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. 2023 Jul 17;10:32. doi: 10.1186/s40779-023-00468-6

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© The Author(s) 2023

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/. 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. 2 — A graphical illustration of how oncogenic and tumor suppressor miRNAs are regulated during tumorigenic events. a When oncogenic miRNAs are expressed at higher levels in malignant cells, tumor suppressor gene expression is lowered either as a result of mRNA degradation or hypermethylation. b Oncogenic miRNA expression may be increased by decreasing the expression level of tumor suppressor miRNAs. Both oncogenic and tumor suppressor miRNAs contribute to tumorigenesis by promoting a variety of malignant phenotypes, including cell development, anti-apoptotic activity, invading, angiogenic, and spreading. RISC RNA-induced silencing complex, ORF open reading frame