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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. 7 — a In WT cancer cells (at least Hela and HepG2), PIWIL2 stabilizes HDAC3 by inhibiting Siah2-mediated degradation. PIWIL2 binding enhances CK2-mediated phosphorylation of HDAC3. As a result, the expression of p53 is reduced followed by a decrease of p21. b In PIWIL2 knockdown cells, p53 has a relative high expression level and p21 as well