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. 2020 Dec 29;19:173. doi: 10.1186/s12943-020-01296-1

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© The Author(s). 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — PTAF overexpression leads to OVCAR-3 cell migration and invasion by regulating miR-25. Wound-healing a and migration assays b showed that PTAF promoted OVCAR-3 cell migration, which was inhibited by forced expression of miR-25. n = 5 independent experiments. *P < 0.05, **P < 0.01. c A Transwell invasion assay showed that PTAF promoted OVCAR-3 cell invasion by regulating miR-25. n = 5 independent experiments. **P < 0.01. Wound-healing d and migration assays e showed that silencing of PTAF inhibited TGF-β1-driven migration in OVCAR-3 cells, which was abated by miR-25 knockdown. n = 5 independent experiments. *P < 0.05, **P < 0.01. f A Transwell invasion assay showed that knockdown of PTAF inhibited TGF-β1-induced OVCAR-3 cell invasion. n = 5 independent experiments. *P < 0.05, **P < 0.01