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. 2019 Sep 2;9:12628. doi: 10.1038/s41598-019-48992-7

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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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Knockdown of HSP60 activates the adenine-AMPK pathway and suppresses the mTOR pathway. (A) Increased phosphorylation of AMPK (T172) in HSP60-KD A2780 cells. (B) Inhibited mTOR pathway in HSP60-KD A2780 cells. (C) Increased p-AMPK and decreased p-mTOR in adenine-treated A2780 cells. p-AMPK and p-mTOR were restored in Compound C-treated HSP60-KD A2780 cells. (D) Cytotoxicity of adenine on A2780 cells. (E) MTDIA, as MTAP inhibitor, could rescue p-mTOR of HSP60-KD cells. (F) Conceptual representation of regulation of the adenine/AMPK/mTOR pathway. Error bars represent ± SEM.