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. 2019 Jun 24;10(7):499. doi: 10.1038/s41419-019-1694-y

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© The Author(s) 2019

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. 4 — a–c CCK-8, colony formation and EdU assays revealed the effect of miR-217 inhibitors on sh-CLRN1-AS1-induced cell proliferation. d Caspase-3 activity test revealed that cell apoptosis suppressed by the knockdown of CLRN1-AS1. e Similarly, we found that autophagy promoted by the inhibition of CLRN1-AS1 was recovered by the cotransfection of miR-217 inhibitor. ^*P < 0.05, ^**P < 0.01 versus control group, indicated data are statistically significant