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. 2018 Aug 30;9(9):888. doi: 10.1038/s41419-018-0882-5

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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–c MTT and colony formation assays demonstrated SNHG5 reversed the growth inhibitory role of miR-26a-5p in HepG2 and MHCC-97L cells. *P < 0.05,**P < 0.01. d, e Transwell invasion assays demonstrated SNHG5 reversed the inhibitory role of miR-26a-5p on invasion in HepG2 and MHCC-97L cells. **P < 0.01. f MTT assays demonstrated GSK3β reversed the growth inhibitory role of SNHG5-shRNA in HepG2 and MHCC-97L cells.**P < 0.01. f Transwell invasion assays demonstrated GSK3β reversed the inhibitory role of SNHG5-shRNA on migration in HepG2 and MHCC-97L cells. **P < 0.01