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. 2021 Feb 17;40:72. doi: 10.1186/s13046-021-01868-z

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© The Author(s) 2021

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. 6 — MiR-154-5p mediates the function of MAPKAPK5-AS1. a-c MTT, colony formation and EdU assays were conducted to explore the effect of miR-154-5p inhibitors on cell proliferation suppressed by MAPKAPK5-AS1 knockdown. d Flow cytometry showed the effect of miR-154-5p inhibitors on apoptosis induced by MAPKAPK5-AS1 knockdown. e-f Transwell assay were performed to evaluate the effects of miR-154-5p inhibitors on the tumor cells abilities of migration and invasion impaired by MAPKAPK5-AS1 kmockdown. c-d Expression of EMT markers was detected by western blotting to assess the effect of miR-154-5p inhibitors on EMT process inhibited by MAPKAPK5-AS1 knockdown. *p < 0.05