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. 2019 Dec 9;77(20):4093–4115. doi: 10.1007/s00018-019-03399-5

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© The Author(s) 2019

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

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Fig. 2 — Binding of HAS3-EVs and their effect on target cell HA secretion, proliferation and invasion. a Effect of short HA oligosaccharides (6–10 monosaccharide units) on binding of EVs originating from HAS3-induced MV3 cells to HaCaT cells. b Effect of melanoma cell-derived EV treatment on HA secretion levels of HaCaT cells. HA secretion was quantified and normalized to RNA content of the cells. Effect of melanoma-derived EVs on the proliferation rate (c, d) and invasion (e, f) in HaCaT (c, e) and WM115 (d, f) cells, respectively. The data represent mean ± S.E. of four independent experiments. *P value < 0.05, **P value < 0.01, one-way ANOVA (Tukey’s test)