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. 2017 Sep 13;7:11501. doi: 10.1038/s41598-017-11914-6

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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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SEMA3C increases migration and invasion in vitro. The migration of RWPE-1-SEMA3C was compared to that of control cells by wound-healing assay. (a) % Migration in wound-healing assay was quantitated by the formula [(pixels at T_0h) − (pixels at T_24h)]/(pixels at T_0h) × 100%. (b) In transwell migration assay, RWPE-1-SEMA3C cells were roughly 3.5 times more motile than control cells; (c) y-axis is fold increase in migration over control cells. In Matrigel Invasion assays, RWPE-1-SEMA3C cells were 2 times more invasive than control cells; (d) y-axis is fold increase in invasion over control cells. RWPE-1-FUGWBW cells migrated more strongly toward SEMA3C (1 μM) than to PBS; (e) y-axis is fold increase in migration over PBS. Data represent mean, ± SD; *p < 0.05 compared to control.