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. 2015 Apr 24;6(17):15610–15627. doi: 10.18632/oncotarget.3639

Figure 4. ENO1 controlled the expression of glycolysis, cell cycle and EMT-associated genes in EC via the PI3K/AKT pathway but not HEEC.

Figure 4

A. Knocking down endogenous ENO1 expression reduced the expression of c-Myc, E2F1, pRb (Ser780) and LDHA, and enhanced p27 in EC cells. However, total Rb was not affected. The expression of Rb, c-Myc, E2F1, pRb (Ser780), p27 and LDHA were not influenced in ENO1 silencing HEEC. B. Suppressing ENO1 expression decreased the expression of EMT marker genes Snail and N-cadherin and enhanced E-cadherin expression. Protein level of E-cadherin was not examined in the HEC-1B cell line. C. Reduced ENO1 expression decreased the expression of pPI3K, and pAKT, as well as p85 and AKT protein levels. The levels of PI3K, AKT, p-PI3K and p-AKT in ENO1 silencing HEEC were not affected. β-actin served as the internal control. Each experiment was repeated three times.