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. 2017 Jul 5;7:4637. doi: 10.1038/s41598-017-04113-w

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© The Author(s) 2017

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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The function of linc-ROR in invasion and migration of HCC cells in vitro was dependent on miR-145. (A) Wound healing assay was performed to determine the mobility capacity of HepG2 cells stably transfected with linc-ROR and HCCLM3 cells stably transfected with shROR in the presence of miR-145/mimics or miR-145/inhibitor, respectively. (B) The metastasis capacity of HepG2 cells stably transfected with linc-ROR and HCCLM3 cells stably transfected with shROR was partially rescued by miR-145/mimics and miR-145/inhibitor, respectively. (C) Western blotting and (D) immunofluorescence analysis of changes in epithelial markers and mesenchymal markers in HepG2 cells stably transfected with linc-ROR and HCCLM3 cells stably transfected with shROR after treatment with miR-145/mimics or miR-145/inhibitor, respectively. Each experiment was performed at least three times. *p < 0.05; **p < 0.01.