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. 2020 Nov 26;20:569. doi: 10.1186/s12935-020-01620-1

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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. 7 — The mechanism graph of regulatory network and function of LINC00152/EZH2/ZEB1. The highly expressed LINC00152 in EC could bind to the PRC2 protein complex (EZH2) to hinder the transcriptional inhibition of the downstream gene ZEB1 and increase the expression of ZEB1 through interaction with EZH2. The overexpression of ZEB1, on the one hand, increases the vimentin (interstitial protein marker) expression and decreases E-cadherin (epithelial protein marker) expression, thereby accelerating EMT; meanwhile, LINC00152 reduces the cleaved PARP and cleaved Caspase 3 expression, resulting in EC cell resistance to L-OHP