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. 2022 Sep 19;20:147. doi: 10.1186/s12964-022-00946-9

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© The Author(s) 2022

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. 6 — Overexpression of AP2 enhances malignancy of lung cancer cells. Overexpression of AP2A (left panel, shown by anti-Flag antibody) and AP2B (right panel, shown by anti-Flag antibody) increased A USP22 Cyclin D1 proteins and B Proliferation in the parental (USP22-WT) but not the USP22-knockout (-KO, −/−) H1299 and A549 cells. C Overexpression of AP2 increased the migration of USP22-WT but not USP22-KO H1299 and A549 cells. D Quantitative data of migration assays. E Overexpression of TFAP2 increased the invasion of USP22-WT but not USP22-KO H1299 and A549 cells. F Quantitative data of invasion assays; *P < 0.05, **P < 0.01 compared to the pcDNA empty plasmid