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. 2022 Nov 12;20:528. doi: 10.1186/s12967-022-03749-1

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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. 7 — p-TBC1D1^Ser660 promoted malignant activities could be inhibited by FZD7 interference. A, B Cell proliferative capability was determined by CCK-8 (A) and EdU (B) assays. C, D Cell metastatic and invasive capability were determined by wound healing (C) and Transwell (D) assays. E TOP/FOP flash assay was conducted on indicate cells to evaluate the effect of FZD7 on WNT/β-catenin signaling. F Western blot analysis was conducted on indicated cells to evaluate the effect of FZD7 on WNT/β-catenin signaling. Data represent mean ± SD of three independent experiments and were analyzed by two-sided unpaired Student’s t-test, *P < 0.05, **P < 0.01