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. 2019 Aug 12;9:11632. doi: 10.1038/s41598-019-48064-w

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© The Author(s) 2019

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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Depletion of SPANXB1 promoted progression of TNBC cells in vitro. Silencing of SPANXB1 (A) reduced migration ((B) low distribution of migrated cells in encircled area), invasion (C) and ROS production (D) by TNBC cells accompanied by enhanced expression of SH3GL2 and decreased expression of FAK, A-Actinin, Vinculin and RAC-1 (A). Mesenchymal to epithelial transition of SPANXB1 depleted TNBC cells ((E) arrows) accompanied by augmented expression of CDH1 and ZO-1 and decreased expression of Snail and Slug in TNBC lines (F). CSi: Control SiRNA; KD: SPANXB1-SiRNA treated. Actin was used as a loading control (A,F). Magnification X 200 (B–E). In Western blotting, all experimental and control antibodies were run in parallel for the same immunoblot. The Image J software (https://imagej.nih.gov/ij/) was used for Western blot quantification and area measurement in the migration assays.