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. 2018 Feb 7;9:545. doi: 10.1038/s41467-018-02951-4

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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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Fig. 3 — SIRT5 promotes colorectal cancer cell growth dependent on its catalytic activity. a, b Western blotting confirming the stable expression of the control vector, FLAG-SIRT5 WT, or FLAG-SIRT5 H158Y in HCT116 (a) and LoVo (b) cells. c, d Growth curve of HCT116 (c) and LoVo (d) cells stably expressing the control vector (blue line), SIRT5 WT (red line), or SIRT5 H158Y (purple line). Data are the mean ± SD of five independent samples. ANOVA with Tukey’s test. ***P < 0.001. N.S. = not significant for the indicated comparison. e Representative wells of the clonogenic growth experiment of HCT116 and LoVo cells stably expressing the control vector, SIRT5 WT, or SIRT5 H158Y, respectively. f, g Quantified data of the clonogenic growth experiment in HCT116 (f) and LoVo(g) cells. Data are the mean ± SD of three independent samples. P values were calculated by ANOVA with Tukey’s test. **P < 0.01 and ***P < 0.001. N.S. = not significant for the indicated comparison