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. 2012 Dec 28;288(6):4076–4084. doi: 10.1074/jbc.M111.317487

FIGURE 2.

FIGURE 2.

Induction of KLF4 mRNA by PPARγ agonists is PPARγ-dependent. A, HT29 and LoVo (wild-type PPARγ) and HCT15 (mutant PPARγ) cells were grown in the absence of serum for 18 h (control (Ctr)) and then incubated with 10 μm TGZ for 24 h. The expression of KLF4 was determined by RT-qPCR and Western blot analysis. Data represent the mean ± S.D. of triplicate experiments. B, HCT116 cells were treated with TGZ or GW9662 or preincubated with 20 μm GW9662 for 30 min and then treated with 10 μm TGZ for 24 h. The levels of KLF4 expression were determined by RT-qPCR and Western blot analysis. C, HCT116 cells were transiently transfected with either pCDE-HA-PPARγ or PPARγ siRNA (siPPARγ) (50 nm) as described under “Experimental Procedures.” After 24 h of transfection, the cells were treated with vehicle (DMSO; −) or TGZ (10 μm; +) for an additional 24 h. PPARγ and KLF4 protein expression was analyzed by Western blotting. β-Actin was used as a loading control. A representative image of three independent experiments is shown.