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. 2017 Apr 3;214(4):1065–1079. doi: 10.1084/jem.20160903

Figure 3.

Figure 3.

AKR1B1 alters the expression of EMT markers and enhances breast cancer cell migration and invasion. (A and B) Expression of AKR1B1, E-cadherin (E-cad), and vimentin was analyzed by Western blotting in MDA-MB231 and SUM159 cells with stable empty vector (Ctr) or knockdown of AKR1B1 expression (shAKR; A), as well as MDA-MB231 and SUM159 cells treated with or without 20 µM epalrestat (Epa; B). (C) Expression of AKR1B1 and E-cadherin was analyzed by Western blotting in T47D and MCF7 cells with stable empty vector or AKR1B1 expression (AKR). (D–F) E-cadherin reporter activity was measured in MDA-MB231 and SUM159 cells with stable empty vector or knockdown of AKR1B1 expression (D) and MDA-MB231 and SUM159 cells treated with or without 20 µM epalrestat (E), as well as T47D and MCF7 cells with stable empty vector or AKR1B1 expression (F). After 48 h, luciferase activities were normalized and determined. (G–J) Migratory ability (G and H) and invasiveness (I and J) of MDA-MB231 and SUM159 cells with stable empty vector or knockdown of AKR1B1 expression (G and I), as well as MDA-MB231 and SUM159 cells treated with or without 20 µM epalrestat (H and J), were analyzed. The percentage of migratory and invasive cells is shown in the bar graphs. Data are mean ± SD in three separate experiments. *, P < 0.01 by Student’s t test.