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. 2023 Apr 14;18:16. doi: 10.1186/s13062-023-00371-z

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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. 4 — mTOR activation of USP5 promotes the proliferation and migration of lung cancer cells. (A) Left, siCtrl, siTSC2 and siTSC2 cells treated with rapamycin were subjected to Western blotting analysis of various proteins of mTOR markers and USP5. Right, siCtrl and siRaptor cells were subjected to Western blotting analysis of various proteins of mTOR markers and USP5. (B) GSEA analysis showed that USP5 high expression was correlated with high Mtorc1 activity in lung cancer patients. (C-E) The proliferation, apoptosis, and migration efficiencies of cells were measured by colony-forming assay, flow cytometry detection, and transwell chamber, respectively, in Ctrl and USP5 overexpressed cells treated with rapamycin. * P < 0.05, ** P < 0.01