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. Author manuscript; available in PMC: 2012 Aug 16.
Published in final edited form as: Oncogene. 2011 Jul 11;31(7):842–857. doi: 10.1038/onc.2011.287

Figure 8. mPGES-1 increases β-catenin DNA binding in Hep3B stable cell lines.

Figure 8

Nuclear extracts were isolated from Hep3B cells stably transfected with different vectors for EMSA (A) or DNA pull down (B-F) with biotin-LEF/TCF oligonucleotide [5′-Biotin-AGATCAAAGGG-3′] (or non-biotinylated cold probe as control), followed by western blotting analysis using specific antibodies as indicated in each panel. WB: Western blotting

A. EMSA showing that mPGES-1 overexpression increased the binding of nuclear protein with LEF/TCF consensus sequence, whereas mPGES-1 knockdown inhibited it.

B. DNA pull down assay showing that mPGES-1 increases β-catenin DNA binding.

C. DNA pull down with co-immunoprecipitation assay showing that mPGES-1 increases β-catenin and EGR1 interaction on TCF/LEF consensus site.

D. DNA pull down with co-immunoprecipitation assay showing that mPGES-1 increases β-catenin and TCF4 interaction on TCF/LEF bind site.

E. DNA pull down assay showing that EGR1 knockdown prevents mPGES-1-induced β-catenin binding to TCF/LEF consensus site.

F. DNA pull down assay showing that β-catenin knockdown prevents mPGES-1-induced EGR1 binding to TCF/LEF consensus site.