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. 2016 Oct 1;11:45. doi: 10.1186/s13020-016-0116-7

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© The Author(s) 2016

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. 11 — Schematic diagram of hypothesized mechanism of trans-FA effect of lung cancer cells. Trans-FA induced ROS leading to degradation of phosphorylated β-catenin. Trans-FA induced regulation of pro-survival proteins survivin and anti-survival protein Bax caused the anti-proliferation of lung cancer H1299 cells. Trans-FA also reduced the activity of both MMP-2 and MMP-9, causing the down-regulation of migration of H1299 cells