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. Author manuscript; available in PMC: 2014 Aug 27.
Published in final edited form as: Oncogene. 2013 Apr 1;33(9):1101–1112. doi: 10.1038/onc.2013.69

Figure 4. 15-PGDH-derived 15-keto-PGE2 activates PPARγ in HCC cells.

Figure 4

A. Enzyme immunoassay (EIA) for 15-keto-PGE2 metabolite in Huh7 stable cell lines. The data are presented as mean±SEM (**p < 0.01 compared to corresponding control).

B. Enzyme immunoassay (EIA) for PGE2 in Huh7 stable cell lines. The data are presented as mean±SEM (*p < 0.05; **p < 0.01).

C. Western blotting for COX-2 in Huh7 cells with stable overexpression or knockdown of 15-PGDH. β-actin was used as the internal control.

D. PPARγ super-EMSA analysis using PPRE probe in Huh7 stable cell lines.

E. DNA pulldown in Huh7 stable cell lines. Biotin and histone were used as pulldown and loading controls.

F. PPRE-luciferase activity assay. a PPRE luciferase reporter activity in Huh7 stable cell lines (**p < 0.01 compared to corresponding control). b PPRE luciferase reporter activity in Huh7 stable cell lines with cotransfection of pCMV6-entry-PGR2 (Origene). c PPRE luciferase reporter activity in Huh7 stable cell lines treated with GW9662 (10µM). d PPRE luciferase reporter activity in wild type Huh7 cells treated with DMSO and 15-keto-PGE2 (10µM, Cayman Chemicals) (with or without PGR2 overexpression or 10µM GW9662 treatment).