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. 2017 Jun 30;7:4469. doi: 10.1038/s41598-017-04736-z

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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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Study of functional characteristics of RAD51-AS1 in cell migration and invasion. (A), Migration assays. The real-time cell indexes indicated that RAD51-AS1 knockdown greatly decreased cell migration capacity compared with the NC cells. Blank control was performed with the bottom chamber containing RPMI 1640 but without FBS as a chemo-attractant. The light-colored error bars denote the SD. (B), Transwell invasion assays. RAD51-AS1 knockdown significantly decreased the invasive capacity of SKOV3, SKOV3.ip and HO8910 cells. (C) Overexpression of RAD51-AS1 increased cell invasion capacity of Hey and OVCAR3 cells. Each experiment was repeated in triplicate (n = 3). (The results are shown as the mean ± SD; *P < 0.05; **P < 0.01; ***P < 0.001 by Student’s t test).