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. 2020 Apr 9;39:61. doi: 10.1186/s13046-020-01551-9

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Knockdown of linc01134 can curb HCC cell migration, invasion and EMT process in vitro and impede metastasis in vivo. a-c Transwell and wound-healing assays were performed to assess cell migration and invasion abilities after knockdown of linc01134. d IF analysis was conducted to investigate the expression of E-cadherin and N-cadherin. e Western blot was conducted to measure EMT-related protein level. f HE staining was conducted to measure the number of metastasis nodes. **P < 0.01