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. 2023 Mar 31;22:66. doi: 10.1186/s12943-023-01743-9

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© The Author(s) 2023

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. 5 — CDR1as activates TGF-β signaling and promotes EMT in cervical cancer cells; A Sanger sequencing shows that overexpressed CDR1as activated TGF-β signaling pathway; B C Western blot shows that P-SMAD2 and P-SMAD3 were upregulated after CDR1as was overexpressed; D Inhibition of TGF-β in CDR1as overexpressed cells reversed the EMT change by Wound healing; E Inhibition of TGF-β in CDR1as overexpressed cells reversed the EMT change by Transwell test