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. 2020 May 12;20:162. doi: 10.1186/s12935-020-01246-3

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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. 2 — CRNDE prominently inhibits cell apoptosis by regulating several relevant effectors. In addition to the miR-384/PIWIL4/STAT3 axis, CRNDE directly regulates miR-136-5p, miR-451, EZH2, FOXM1, PAK7, XIAP and other genes to inhibit apoptosis as well. CRNDE is also involved in the controlling processes via caspase family, Bcl-2 family and some tumor suppressors, such as caspase3, Bcl-2, Bcl-xL, Bax, BAD, MARK2, CDKMA and DUSP5 et al., suppressing apoptosis