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. 2018 Feb 20;8:3317. doi: 10.1038/s41598-018-21570-z

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© The Author(s) 2018

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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Shikonin inhibits both C-MYC and PI3K/AKT/mTOR activity in vitro. (A) Western blot indicated the protein expression of C-MYC in BL cells after treatment with SHK. β-actin was used as a loading control. (B) and (C) Namalwa and Raji cells were treated with SHK for 12 h. The relative expression of miR-19a was analyzed by RT-PCR. Data are presented as the mean ± SD of three independent experiments. (D) Western blot indicated the protein expression of phosphorylation of PI3K/AKT/mTOR in BL cells after treatment with SHK. β-actin was used as a loading control. (E) The protein expression of C-MYC was analyzed by western blot after treatment with C-MYC inhibitor 10058-F4 (100 uM) in BL cells. β-actin was used as a loading control. Cropped blots/gels were used in the figure and the gels had been run under the same experimental conditions; the fulllength blots/gels are presented in Supplementary Figure S2. (F) RT-PCR was performed to evaluate the effect of 10058-F4 (100 uM) on expression of miR-19a in Namalwa cells. All data represent an independent experiment from three repeated tests with similar results.