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. 2018 Mar 6;37:49. doi: 10.1186/s13046-018-0717-3

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 7 — PPAR-γ/AKT signaling is essential for the biological function of miR-1468 in HCC. a Hep3B and MHCC-97 L cells that were transfected with corresponding miRNA vectors were subjected to immunoblotting for phosphorylated AKT and AKT. PPAR-γ agonist rosiglitazone treatment inhibited the promotive effects on cell proliferation (b, c), colony formation (d), cell cycle progression (e) and apoptosis (f) of miR-1468 overexpressing Hep3B cells. PPAR-γ antagonist, T0070907, reversed the suppressive effects of miR-1468 knockdown in MHCC-97 L cells. g Western blot analysis indicated that modulating PPAR-γ activation reversed the effects of miR-1468 alteration on cell cycle and apoptosis associated factors of HCC cells. *P < 0.05