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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. 8 — PLAGL2/EGFR/AKT pathway mediates the oncogenic effect of MAPKAPK5-AS1. a-c MTT, colony formation and EdU assays showed the effect of PLAGL2 on cell proliferation suppressed by MAPKAPK5-AS1 knockdown. d Flow cytometry showed the effect of PLAGL2 on cell apoptosis induced by MAPKAPK5-AS1 knockdown. e Transwell assay showed the effects of PLAGL2 on migration and invasion of the tumor cells suppressed by MAPKAPK5-AS1 knockdown. f Expression of EMT and EGFR/AKT pathway markers was detected by western blotting to assess the effect of PLAGL2 on EMT process and pathway activity inhibited by MAPKAPK5-AS1 knockdown. *p < 0.05