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. 2024 Jul 29;43:211. doi: 10.1186/s13046-024-03119-3

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© The Author(s) 2024

Open Access This 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 — pIGF1R promotes EMP acquisition in epithelial cSCC cancer cells. A, B Hierarchical cluster analysis of differentially phosphorylated peptides (FDR p < 0.05) (A) between full epithelial and EpCAM⁺ plastic cancer cells isolated from WD-SCCs and MD/PD-SCCs, respectively, and (B) between EpCAM⁺ plastic and EpCAM^neg cancer cells isolated from MD/PD-SCCs (n = 3/group). C Venn diagram of the number of proteins specifically phosphorylated in the EpCAM⁺ plastic signature compared with full epithelial and EpCAM^neg cancer cells. D Percentage (mean ± SD) of GFP⁺pIGF1R⁺ cancer cells in epithelial (n = 5), mixed (n = 5), and mesenchymal (n = 4) cSCCs, determined by IF assays. P-value (one-way ANOVA with Tukey’s test). E Western blot confirmation of IGF1R knockdown in EpCAM^high sh-IGF1R (1) cancer cells prior to engraftment into immunocompetent syngeneic mice. Actin was used as a loading control. F Growth kinetics (mean ± SD) of EpCAM^high sh-control and sh-IGF1R (1)-derived tumors (n ≥ 18/group). P-value (Repeated Measures ANOVA test). G Representative image of IGF1R levels in the indicated cancer cells after tumor growth. Actin was used as a loading control. H Percentage (mean ± SD) of EpCAM^high, EpCAM^low, and EpCAM^neg cancer cells generated after the engraftment of EpCAM^high sh-control (n = 18) and sh-IGF1R (1) (n = 20) cancer cells into immunocompetent syngeneic mice. P-value (unpaired two-tailed Student’s t-test). I, J (I) Percentage (mean ± SD) of ITGAV⁺ cancer cells and (J) median ITGAV intensity (mean ± SD) of cancer cells in EpCAM^high sh-control and sh-IGF1R (1)-derived tumors. P-value (unpaired two-tailed Student’s t-test). K pSMAD3 levels after TGFβ1 (2.5 ng/µl) treatment for 14 days in the indicated cancer cells. Actin was used as a loading control. L Percentage (mean ± SD) of EpCAM^high, EpCAM^low, and EpCAM^neg cancer cells generated in TGFβ1-treated (+) and untreated (-) EpCAM⁺ plastic sh-control (n = 4) and sh-IGF1R (1) (n = 3) cancer cells. P-value (unpaired two-tailed Student’s t-test). M Median ITGAV intensity (mean ± SD) of sh-control (n = 4) and sh-IGF1R (1) (n = 3) cancer cells treated with TGFβ1 relative to their respective untreated controls. P-value (unpaired two-tailed Student’s t-test)