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. 2021 Jun 9;21:680. doi: 10.1186/s12885-021-08402-6

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© The Author(s) 2021

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. 8 — A model of A1542/A1543-mediated suppression of leukemia via cholesterol biosynthesis and role of latter in other types of cancer. a Activation of ERK/MAPK by ERK1/2 agonist A1542/A1543 induces genes including SREBPs, EGR1 and AP1 (JUN-FOS) involved in cholesterol biosynthesis, as well as other death promoting signals, together responsible for leukemia inhibition in culture and in vivo. b TCGA analysis of renal cancer survival as a function of elevated cholesterol biosynthesis genes