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. 2018 Nov 9;18:176. doi: 10.1186/s12935-018-0671-3

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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. 6 — IL-2 and sorafenib co-treatment regulated mitochondrial fission via the JNK-TAZ pathways. a–c JNK phosphorylation and TAZ expression were measured via western blotting. SP600125, an inhibitor of JNK, was used to inhibit the activity of the JNK-TAZ pathways. d, e Mitochondrial fission was observed via immunofluorescence, and the average length of the mitochondria was recorded. f–h The regulatory effects of IL-2 and sorafenib co-treatment on the JNK-TAZ pathways and mitochondrial fission were monitored via immunofluorescence. IL-2 and sorafenib co-treatment promoted the upregulation of JNK phosphorylation, which was accompanied by an increase in Drp1, a factor for mitochondrial fission. *P < 0.05 vs. control group; ^@P < 0.05 vs. IL-2+ sorafenib group. Cont control