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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 cooperates with p53 and works with etoposide to further inhibit HCT116 tumor growth. After nude mice injecting HCT116 cells for 1 week, the mice were i.p. injected with etoposide (8 mg/kg) or PBS for 5 consecutive days. Afterward, the mice were fed with Oligo-Fucoidan (300 mg/kg) or PBS orally thrice a week for 5 weeks. The effects of single and combination therapies on tumor growth of the p53^+/+ cell-bearing mice (a) and the p53^−/− cell-bearing mice (b) were assessed. The results of HCT116 tumor burdens after different treatments were analyzed (c). Histograms show the therapeutic effects of the indicated treatments in HCT116 tumor-bearing mice (d). The tumor-promoting M2 macrophages (indicated by dashed circles) identified in TME of the mice-bearing p53^+/+ and p53^−/− tumors were examined by immunohistochemistry of CD163 expression (e). Scale bar represents 20 μm.