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. 2022 Jan 3;41:6. doi: 10.1186/s13046-021-02212-1

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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 — IGF2BP2 promotes metastatic behaviour of HNSCC cells in vitro. A-B The efficiency of knockdown and overexpression of IGF2BP2 was validated by RT-qPCR (A) and western blot (B) at mRNA as well as protein levels in FaDu and SCC15 cells. GAPDH served as an internal control. ***P < 0.001, ****P < 0.0001, ns: not statistically significant. C-D Images representing wound healing (C) and transwell assays (D) showing the mobility and invasiveness of HNSCC cells after knockdown or overexpression of IGF2BP2. Lower right panel shows the statistical data of cell migration distance, and migrated and invaded cell counts. *P < 0.05, **P < 0.01, ***P < 0.001. All the data are presented in the form of mean ± SD from three independently performed experiments