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. 2021 Oct 16;21:537. doi: 10.1186/s12935-021-02245-8

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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. 10 — Effects and mechanisms of miR-140-3p on the growth and metastasis of GC. First, miR-140-3p directly bound to SNHG12 in GC and thus down-regulated the expression of SNHG12and reduced the binding of SNHG12 and HuR, inhibiting the transportation of HuR from the nuclei to the cytoplasm. Therefore, the binding of HuR and FAM83B mRNA was inhibited and FAM83B mRNA’s stability was reduced, and the transcription of FAM83B was down-regulated. Furthermore, the proliferation, invasion, and migration of GC cells were inhibited and the growth and metastasis of GC were inhibited