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. 2021 Aug 16;6:303. doi: 10.1038/s41392-021-00714-0

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© The Author(s) 2021

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. 6 — HDAC4 and HDAC5 regulate the acetylation of SerRS in breast cancer cells. a, b The MDA-MB-231 cells (a) and MCF 10A cells (b) were treated with SIRT inhibitor nicotinamide (NAM, 10 mM), SIRT1 inhibitor selisistat (EX-527), and SIRT2 inhibitor thiomyristoyl (TM) at indicated dosages for 48 h and the nuclear and cytoplasmic SerRS were analyzed by western blot. Quantification results are shown as means ± SEM from three independent experiments (ns indicates not significant, by unpaired Student’s t-test). c The MDA-MB-231 cells were treated with HDAC inhibitor trichostatin A (TSA, 1 μM), HDAC1 and HDAC3 inhibitor entinostat (MS-275, 10 μM), HDAC6 inhibitor Tubastatin A (10 μM), NAM (10 mM) and DMSO control for 48 h and the nuclear and cytoplasmic SerRS were analyzed by western blot. Quantification results are shown as means ± SEM from three independent experiments (***P < 0.001, by unpaired Student’s t-test). d Western blot analysis of nuclear translocation of SerRS in MDA-MB-231 cells treated with TSA and specific HDAC4 and HDAC5 inhibitor LMK-235 at indicated dosages. Quantification results are shown as means ± SEM from three independent experiments (***P < 0.001, by unpaired Student’s t-test). e SerRS acetylation in MDA-MB-231 cells treated with indicated dosages of TSA and LMK-235 were analyzed by western blot. Quantification results are shown as means ± SEM from three independent experiments (*P < 0.05, **P < 0.01, by unpaired Student’s t-test). f Western blot analysis to show that HDAC4 and HDAC5 in MDA-MB-231 cells were specifically silenced by shRNAs, i.e., shHDAC4 and shHDAC5. A shRNA targeting LacZ (shLacZ) was used as a negative control. Quantification results are shown as means ± SEM from three independent experiments (***P < 0.001, by unpaired Student’s t-test). g HDAC4 and HDAC5 were silenced by specific shRNAs and the nuclear translocation of SerRS was analyzed by western blot. Quantification results are shown as means ± SEM from three independent experiments (*P < 0.05, by unpaired Student’s t-test)