Fig. 5

SHH002-hu1 enhances the ability of Bevacizumab to inhibit MDA-MB-231/MDA-MB-468 tumor growth significantly. a. Representative images of isolated tumors from MDA-MB-231 (the left 5 rows)/MDA-MB-468 (the right 5 rows)-tumor bearing nude mice. b. MDA-MB-231/MDA-MB-468 tumor growth curves of each group under different treatments. Data were given as the mean ± SD (n = 5), ^*p < 0.05, ^**p < 0.01. c. Bevacizumab induced hypoxia in TNBC tumor tissues in vivo, and ALDH1⁺ cells were concentrated in hypoxic regions. Hypoxia in MDA-MB-231/MDA-MB-468 tumors was detected by IF staining of pimonidazole adducts in sections from different groups. Staining showed pimonidazole immunodetection (green) and ALDH1 (red) merged with DAPI-stained nuclei (blue), bar = 100 μm. d. The β-catenin pathway of MDA-MB-231/MDA-MB-468 tumor was stimulated in response to hypoxia after the treatment of Bevacizumab. Staining showed pimonidazole immunodetection (green) and β-catenin (red) merged with DAPI-stained nuclei (blue), bar = 100 μm. e. IF stainings of ALDH1 (red) were shown, and nuclei were counterstained with DAPI (blue), bar = 100 μm. f. Quantitation of ALDH1⁺ cells in control/Bevacizumab-treated/Bevacizumab + SHH002-hu1-treated tumors. Data were shown as mean ± SD (n = 5), ^*p < 0.05, ^**p < 0.01. g. SHH002-hu1 repressed the accumulation of β-catenin in the nucleus induced by Bevacizumab. IF stainings of β-catenin (red) were shown, and nuclei were counterstained with DAPI (blue), bar = 50 μm