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. 2017 Sep 12;7:11277. doi: 10.1038/s41598-017-11842-5

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© The Author(s) 2017

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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OA inhibits the Akt/mTOR signaling pathway. (a) Western blot displaying the expression levels of Akt, p-Akt, mTOR, p-mTOR, PTEN, p-S6K, p-4E-BP1, p-ERK1/2, and ERK1/2 in CAL27 and UM1 cells after treatment with OA for 24 h. GAPDH was used as the internal control. (b–e) The protein expression levels from the above Western blot were quantitated. Bar graphs showed that the p-Akt/Akt ratio and p-mTOR/mTOR ratio were significantly decreased after treatment with OA. OA induced a decreased in p-Akt protein expression from 2.1-fold to 0.9-fold and from 3.2-fold to 1.2-fold in CAL27 and UM1 cells, respectively. p-mTOR expression was decreased from 0.78-fold to 0.59-fold in CAL27 cells and from 0.6-fold to 0.2-fold in UM1 cells. The results are presented as the mean ± standard deviation for three independent experiments (**p < 0.01, ***p < 0.001).