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. 2018 May 24;9(6):627. doi: 10.1038/s41419-018-0646-2

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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. 5 — a Expression of CK1ε in RCC cells following stable knockdown of REGγ. b Expression of CK1ε in RCC cells following REGγ knockdown by small interfering RNA. c, d The stability of CK1ε was assessed by CHX treatment for indicated time in RCC cells following REGγ depletion. e The correlation between CK1ε and REGγ expression in RCC tissue samples revealed by IHC staining. Scale bar = 50 μm. f, g The suppressive effect of REGγ depletion on RCC cells growth was partly abolished by CK1ε knockdown as determined by MTT assay. h, i The promotion of REGγ depletion on RCC cells apoptosis was partly reversed by CK1ε knockdown as determined by flow cytometry. Data are shown as mean ± SD. *P < 0.05