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. 2019 Feb 11;10(2):117. doi: 10.1038/s41419-019-1363-1

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Promoter activity was determined in HEK293T cells transfected with miR145-Luc (0.2 µg) and indicated plasmids. (b–d) Immunoblotting for Fli-1 (b) mRNA (c) or (d) miR145 following transduction of the sh-Fli-1 lentivirus. e Promoter sequence of FLI1 with the FLI1 binding sites (FBS1-3) highlighted in red. e, f Chromatin immunoprecipitation (ChIP) analysis for the regions containing FBS1 (f) and FBS2-3 (g). h Depicted model of A661/A665. In leukemic cells, high Fli-1 suppresses of the miR-145 promoter, leading to higher Fli-1 expression. The diterpenoid compounds A661 and A665 suppress Fli-1 expression either directly or through an upstream factor. Fli-1 downregulation in turn depresses the miR-145 promoter, thereby leading to miR145-mediated inhibition of Fli-1 translation