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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Mol Cancer Res. 2010 May 25;8(6):833–843. doi: 10.1158/1541-7786.MCR-09-0400

Figure 2.

Figure 2

Figure 2

The Spry4 promoter is activated by PPARγ expression. (A) H157 and H2122 cells with stable Wnt7A and/or Fzd9 expression were transfected with Spry4-luciferase. Results are the average of triplicate experiments. (B) H157 and H2122 cells were transiently transfected with PPAR response element (PPRE) –luc, Spry4 and wild type PPARγ. H157 and H2122 cells were transfected with wild type PPARγ and Spry4 promoter luciferase and treated with T007, a PPARγ inhibitor. Results are the average of triplicate experiments. (C) H157 and H2122 cells with stable PPARγ expression were transfected with full length (−4446) and truncated versions of Spry4-luciferase (−1182, −418, −31). Results are the average of triplicate experiments. Change in activity is presented as fold-induction of the luciferase reporter.