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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Tumor-derived exosomal ADAM17 promotes pre-metastatic niche formation by enhancing vascular permeability in colorectal cancer

Fig. 4

EMT-CRC exosomes enhance tumor metastasis by regulating VE-cadherin expression in vivo. (a) Schematic illustration of the tumor metastasis experiments used to assess Nor-HCT116-Exo- and EMT-HCT116-Exo-treated mice. (b) Representative immunohistochemistry staining of VE-cadherin and immunofluorescence staining of CD34/VE-cadherin at the invasive front in mice with CRC (black scale bar = 50 μm, white scale bar = 25 μm). (c) Analysis of Nor-HCT116-Exo and EMT- HCT116-Exo treated mice, showing relative VE-cadherin levels at the invasive front (n = 10), CTC counts (n = 20), and percentage of mice with both lung and liver metastasis. (d) Representative H&E staining results of lung sections from Nor-HCT116-Exo- and EMT-HCT116-Exo-treated mice. Arrows indicate tumor nodules. Scale bar = 250 μm. (e) Evans blue accumulation in the lung parenchyma (n = 8). (f) The percentage of mice with lung metastasis, alongside the number and maximal diameter of metastatic nodules in the lungs of Nor-HCT116-Exo- and EMT- HCT116-Exo-treated mice. (g) Representative H&E staining results of liver sections from Nor-HCT116-Exo- and EMT-HCT116-Exo-treated mice. Arrows indicate tumor nodules. Scale bar = 250 μm. (h) Evans blue accumulation in the liver parenchyma (n = 8). (I) Percentage of mice with liver metastasis, alongside the number and maximal diameter of metastatic nodules in the liver of Nor-HCT116-Exo- and EMT-HCT116-Exo-treated mice. Data are expressed as mean ± standard deviation. *P < 0.05, **P < 0.01, compared with the control group

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