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. 2014 Oct 13;111(43):15526–15531. doi: 10.1073/pnas.1407717111

Fig. 2.

Fig. 2.

PKM2 is required for EMT induction. (A) Phase-contrast photomicrographs of SW480 cells transfected with siControl or siPKM2 after EMT induction for 48 h. (B) Relative transcript (mRNA) levels of CDH1 and VIM after EMT induction in cells transfected with siControl or siPKM2 for 48 h. (C) Western blot assays of E-cadherin, vimentin, PKM2, and β-actin expression in pre-EMT and post-EMT cells. Post-EMT cell samples were harvested at 72 h. With normalization to β-actin as a control, the relative intensities of E-cadherin and vimentin are shown in comparison with those in the control pre-EMT condition. Note that siPKM2 knockdown works efficiently in post-EMT cells. (D) Invasive behavior of SW480 cells treated with siControl or siPKM2. (E) Schematic procedure for establishing PKM1 OE or PKM2 OE SW480 cells. (F) Western blot assays of PKM1, PKM2, and β-actin expression in WT SW480 cells, cells stably expressing shRNA constructs targeting pyruvate kinase (shPK), and shPK cells overexpressing either PKM1 or PKM2 constructs. (G) Relative mRNA levels of CDH1, VIM, and ZEB1 after EMT induction in PKM1 OE or PKM2 OE SW480 cells for 72 h. (H) Western blot assays of E-cadherin, vimentin, and β-actin expression in PKM1 OE and PKM2 OE cells. Post-EMT cell samples were harvested at 72 h. Column values = average of at least three independent experiments; error bars represent SD from the mean of triplicate experiments. *P < 0.05.