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. 2020 Oct 24;11(10):912. doi: 10.1038/s41419-020-03121-5

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© The Author(s) 2020

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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Fig. 5 — A The wound width was decreased under the treatment of miR-488 inhibitor, consistent with the level of FSCN1, and the wound healing abilities was resuppressed when knockdown the expression of FSCN1 in MCF-7-miR-488-inhibitor cells. B The migration and invasion abilities were consistent with the wound healing abilities, reflecting the motility of MCF-7 cells, which was suppressed in siFSCN1+miR-488 inhibitor-treated cell compared with miR-488 suppressing function. C The wound healing rate was decreased by miR-488 mimic, and the reverse effect was found in the re-overexpression of FSCN1 in MDA-MB-231 cells. D The migration and invasion abilities were consistent with the wound healing assays, predicting the motility of MDA-MB-231, which was promoted by re-overexpression of FSCN1 compared with the NC group.*p < 0.05, **p < 0.01, and ***p < 0.001.