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. 2017 Sep 19;7:11864. doi: 10.1038/s41598-017-12111-1

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© The Author(s) 2017

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Oligo-Fucoidan suppresses IL-6 and CCL2 production as well as STAT3 and STAT5 activation. (a) HCT116 cells were treated with etoposide (40 μM) alone or etoposide and Oligo-Fucoidan (400 μg/ml) for 24 h. IL-6 and CCL2 secretion was measured after the cells were incubated in treatment-free and serum-free medium for 48 h. The results represent the mean ± SD of three independent experiments. *p < 0.05; **p < 0.001. (b) STAT3 (Ser727) and STAT5 (Ser726/731) phosphorylation was analyzed after the above cells were treated with etoposide alone or Oligo-Fucoidan and etoposide for 24 h. (c) The cells were studied after being treated with etoposide for 18 h or pre-treated with Oligo-Fucoidan for 6 h before being treated etoposide for another 18 h. (d) The cells were characterized after etoposide treatment for only 6 h or followed by Oligo-Fucoidan treatment for 18 h. STAT3 (Ser727) and STAT5 (Ser726/731) phosphorylation levels were individually normalized to total STAT3 and STAT5 levels. The corresponding expression levels of STAT3 and STAT5 in the MOCK-treated group were defined as 1.