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. 2020 Aug 15;20:394. doi: 10.1186/s12935-020-01481-8

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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 — KCNQ1OT1 essentially maintained the malignant phenotypes of PC cells by targeting miR-15a. a–c The apoptosis (a), migration (b), and invasion (c) of indicated PC cells were examined by Annexin V/PI dual staining followed by flow cytometry, wound healing assay, and Transwell assay, respectively. d The protein levels of Ras, p-ERK1/2, ERK1/2, Snail, E-cadherin, N-cadherin and MMP-9 were examined by western blot. DU145 and PC-3 cells were not transfected or transfected with shNC, shKCNQ1OT1, shKCNQ1OT1 + inhibitor NC, or shKCNQ1OT1 + miR-15a inhibitor, respectively. *P < 0.05 and **P < 0.01