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. 2022 Sep 14;8:384. doi: 10.1038/s41420-022-01177-0

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© The Author(s) 2022

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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Fig. 6 — A Transwell (scale bars = 100 μm), B colony-formation, C wound healing (scale bars = 50 μm), D CCK-8, and E apoptosis assays revealed the effect of miR-16-5p inhibitor on promoting cell migration and growth, while it inhibited apoptosis, and ABL2 siRNA mitigated it. F As revealed by Western blotting assay, miR-16-5p inhibitor increased ABL2 expression. G and H ABL2 silencing within MGC-803 cells decreased N-Cadherin, Vimentin, Snail, YAP, and p-SMAD2/3 levels, while no change was observed for SMAD2/3. I–K miR-16-5p upregulation can alleviate GC cells biological behaviors with ABL2 downregulation. L MiR-16-5p mimics reduces the role of Arg lentiviral activation particles. M and N Western blotting detected the effects of miR-16-5p mimics and Arg lentiviral activation particles effects on EMT and SMAD2/3, p-SMAD2/3, YAP, and p-YAP protein levels. *p < 0.05, **p < 0.01, ***p < 0.001.