Fig. 2

AKR1B10 promotes the proliferation, migration and invasion of breast cancer cells in vitro via regulation of epithelial-mesenchymal transition (EMT) and proliferation-related genes. A, B RT-PCR and western blot analysis of gene expression changes upon AKR1B10 overexpression and knockdown in MCF-7 cells and BT-20 cells, respectively; C, D AKR1B10 overexpression increased cell proliferation in MCF-7 cells and AKR1B10 knockdown inhibited cell proliferation in BT-20 cells; E, F MCF-7 cell migration was significantly enhanced when AKR1B10 was overexpressed while BT-20 cell migration was significantly inhibited when AKR1B10 was knocked down in a scratch wound assay; G Migration and invasion ability of MCF-7 cells after AKR1B10 overexpressing in a transwell assay. H Migration and invasion ability of BT-20 cells after AKR1B10 knocking down in a transwell assay. I, J Western blotting analysis showed increased protein levels of c-myc, cyclinD1, and Survivin in MCF-7/AKR1B10 cells, and reduced protein levels in BT-20/shAKR1B10#1 cells, respectively; K Western blotting analysis showed significantly upregulated ZEB1, SNAI1, SLUG, Twist and downregulated E-cadherin in MCF-7/AKR1B10 cells compared to vector control cells; L Western blotting analysis showed significantly reduced ZEB1, Twist at protein level in BT-20/shAKR1B10#1 cells compared to scramble control cells. Experiment was repeated three times. Representative results were presented. *P < 0.05