Epithelial to mesenchymal transition in arsenic-transformed cells promotes angiogenesis through activating β-catenin-vascular endothelial growth factor pathway

Zhishan Wang; Brock Humphries; Hua Xiao; Yiguo Jiang; Chengfeng Yang

doi:10.1016/j.taap.2013.04.018

Fig. 3

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Stably re-expressing miR-200b in arsenic-transformed cells restores β-catenin cytoplasmic membrane localization and reduces its target gene expression

(A) Representative images of arsenic-transformed vector control cells (As-p53^lowHBEC-GFP) shown in a bright field (upper panel) and their β-catenin immunofluorescence staining (lower pane). White arrows point to representative nucleus stainings of β-catenin. (B) Representative images of arsenic-transformed miR-200b stably expressing cells (As-p53^lowHBEC-GFP-200b) shown in a bright field (upper panel) and their β-catenin immunofluorescence staining (lower pane). White arrows point to representative cytoplasmic membrane stainings of β-catenin. β-Catenin immunofluorescence staining was carried out as described in Materials and Methods. Scale bar=50 μm. (C) Representative Western blot analysis of cellular β-catenin, c-myc, cyclin D1 and VEGF protein levels. Western blot was carried out as described in Materials and Methods. (D) Q-PCR analysis of cellular c-myc, cyclin D1 and VEGF mRNA levels (means ± standard deviations, n=3). Q-PCR analysis was performed as described in Materials and Methods. * p<0.05, compared to the As-p53^lowHBEC-GFP cells. Similar results were obtained in two additional experiments.