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. 2021 May 22;11:94. doi: 10.1186/s13578-021-00600-w

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© The Author(s) 2021

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. 3 — The molecular regulatory mechanisms for MET in OS cells. The EMT-inducing transcription factors including SNAIL, SLUG, TWIST1 and ZEB1 are expressed in OS cells, which directly or indirectly repress the expression of epithelial genes such as E-cadherin to maintain mesenchymal cell features. MET is initiated by inhibiting EMT-TFs through activating upstream signaling pathways such as SYT-SSX1/2, OVOL2 and miRNAs or suppressing AMF/PGI or LRP5 in OS cells. Please refer to the text for related references. VDR vitamin D receptor, TIMP1 TIMP metallopeptidase inhibitor 1