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. 2020 Aug 3;20:360. doi: 10.1186/s12935-020-01447-w

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© The Author(s) 2020

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-326 exerted its role through SMAD6 in HCC cells. a Western blot analysis was conducted to assess the influence of SMAD6 overexpression on SMAD6 protein levels of miR-326-elevated HCCLM3 and Huh7 cells. b–f Impacts of SMAD6 augmentation on miR-326 enhancement-mediated proliferation, colony formation, cell cycle, migration, and invasion of HCCLM3 and Huh7 cells were determined with CCK-8 (b), colony formation (c), flow cytometry (d), wound healing (e), or transwell assays (f). g, h Effects of SMAD6 overexpression on the levels of Cyclin D1, MMP2, and MMP9 of miR-326-elevated HCCLM3 and Huh7 cells were evaluated via western blot analysis. *P < 0.05