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. 2018 Mar 19;9(4):423. doi: 10.1038/s41419-018-0462-8

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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. 6 — a PIWIL2 knockdown reduces the binding of HDAC3 and increases Ac-H3 level on P53 promoter. b HDAC3 overexpression recovers the up-regulation of p53 and p21 by PIWIL2 knockdown. c, d In Hela cells, HDAC3 inhibition eliminates the effect of PIWIL2 on cell proliferation while HDAC3 overexpression recovers the impact of PIWIL2 knockdown on cell proliferation (P < 0.05). e, f HDAC3 inhibition eliminates the inhibition role of PIWIL2 on cell apoptosis. (P < 0.05)