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. 2022 Oct 3;132(19):e157399. doi: 10.1172/JCI157399

Figure 1. Bevacizumab treatment induces vessel co-option and FAPα expression in the co-opted HSCs in CRCLM xenografts.

Figure 1

(A) Schematic showing the strategy for generating the bevacizumab-resistant CRCLM xenografts. Tumors were harvested and photographed at the end of experiments. (B) H&E staining of the tumor-liver interface of CRCLM xenografts. Scale bar: 100 μm. Quantification of RHGP is shown (n = 6). (C) Immunofluorescence staining of the EpCAM+ tumor cells (green) that infiltrated the liver parenchyma and hijacked the CD31+ sinusoidal blood vessels (red) in the tumor-liver interface of CRCLM xenografts. Scale bar: 50 μm. Quantification of the co-opted sinusoidal blood vessels is shown (n = 6). (D) Immunofluorescence staining of FAPα (gray) in αSMA+ HSCs (green) attached to the CD31+ sinusoidal blood vessels (red) in the CRCLM xenografts. Scale bar: 20 μm. Dotted lines indicate the tumor-liver interface. LM, liver metastases; T, tumor; L, liver; Bev AR, bevacizumab acquired resistance; Bev IR, bevacizumab intrinsic resistance. Data are presented as mean ± SEM. NS, no significance. ***P < 0.001 (2-tailed, unpaired t test).