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. 2021 Jan 11;16:5. doi: 10.1186/s13000-020-01063-2

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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. 4 — PTEN directly mediated the regulatory effects of miR-324-5p on AGS cell proliferation, apoptosis, migration and invasion. a. The putative binding site of miR-324-5p at the 3′-UTR of PTEN. b. The relative luciferase activity in AGS cells in the dual-luciferase reporter assay. c. The mRNA expression of PTEN was inhibited by miR-324-5p overexpression, and the pcDNA3.1-PTEN could reverse this effect. d-g. The promoted cell proliferation, inhibited cell apoptosis and enhanced cell migration and invasion induced by miR-324-5p overexpression were all abolished by the upregulation of PTEN in AGS cells. *P < 0.05, **P < 0.01, ***P < 0.001 compared to control group; ^#P < 0.05, ^##P < 0.01 compared to miR-324-5p mimic group