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. 2018 Jan 12;8:606. doi: 10.1038/s41598-017-18739-3

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© The Author(s) 2018

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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FOSL2 downregulation is a critical step in regulation of OS properties by miR-143-3p. (A) The miR-143-3p expression after transfected with lentivirus vectors. (B) (left) MG-63-miR cell (stably express miR-143-3p) were transfected with empty pcDNA3.1 vector, FOSL2-containing plasmid; (right) MG-63-miR cell were transfected with siRNA against FOSL2. (C) Cell viability of the two cell lines were measured by CCK-8 assay. The results showed that cell viability of ectopic FOSL2 group was higher than the control group. And the cell viability of siFOSL2 group was lower than NC group. (D) Cell cycle distribution were measured by flow cytometry analysis. The effects of G1/S phase blocking was weakened by ectopic FOSL2 and enhanced by siFOSL2. (E) Image and quantification of cell invasion ability were measured by Transwell assay.