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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: A novel humanized Frizzled-7-targeting antibody enhances antitumor effects of Bevacizumab against triple-negative breast cancer via blocking Wnt/β-catenin signaling pathway

Fig. 7

SHH002-hu1 reduces the adaptability of TNBC to hypoxia. a. IF assay of CD31 staining (red) indicated that SHH002-hu1 enhanced the anti-angiogenesis effect of Bevacizumab against TNBC, bar = 100 μm. b. IHC assay of PAS/CD31 double staining after drug discontinuation showed that the number of VM channels (red arrows) increased in the Bevacizumab group compared to the control, and the endothelium-dependent vessels (yellow arrows) rebounded after Bevacizumab discontinuation. SHH002-hu1 inhibited VM and the endothelium-dependent vessels rebound induced by Bevacizumab significantly. c. Western blot assay showed that the VM-associated proteins VE-cadherin and Twist1 were upregulated in the Bevacizumab-treated MDA-MB-231/MDA-MB-468 tumors, and SHH002-hu1 obviously suppressed the phenomenon. d. The HIF-1a transcriptional activity was enhanced by hypoxia remarkably, and SHH002-hu1 effectively inhibited the HIF-1a transcriptional activity under hypoxic condition. Data were presented as the mean ± SD, n = 3, *p < 0.05, **p < 0.01. e. Western blot assay showed that the expression of HIF-1a and HIF-1a targets (VEGFA, Glut1) was enhanced by hypoxia, and SHH001-hu1 could suppress the expression of VEGFA/Glut1 through inhibiting the expression of β-catenin under hypoxic condition

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