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. 2015 Oct 19;6(36):38967–38982. doi: 10.18632/oncotarget.5734

Figure 5. AKR1B10 is involved in regulating EMT.

Figure 5

Vimentin, N-cadherin, E-cadherin and AKR1B10 expressions were determined by Western blot analysis in Huh-7, Huh-7-Luc, and highly invasive (Huh-7-I1, Huh-7-I2, Huh-7-I3 and Huh-7-I4) cells. Actin was used as a loading control. B. Control and 14-3-3ε stable cells were transfected with scramble and two sequences of AKR1B10 siRNAs for 48 hrs. Vimentin, N-cadherin, Zeb-1, snail and E-cadherin expressions were determined by Western blot analysis. Actin was used as a loading control. C. Huh-7-I1 cells were transfected with control and AKR1B10 overexpression vectors for 48 hrs. AKR1B10 expression was examined by Western blotting analysis and actin was used as a loading control (upper panel). Effect of AKR1B10 overexpression on cell migration (middle panel) and invasion (lower panel) was determined by Boyden chamber assay. Scale bars: mean ± SD. **, P < 0.01. D. An illustrated scheme for potential roles of 14-3-3ε and AKR1B10 in regulating HCC tumor progression.