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. 2009 Sep 15;284(47):32483–32492. doi: 10.1074/jbc.M109.014589

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© 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 8. — Mechanisms of MIF-GCs interactions in U373 MG glioma cells (continuous arrows) and inflammatory models (dashed arrows). GCs decrease cell proliferation, migration, and invasion through a GR-dependent mechanism and inhibit the ERK1/2 MAPK pathway by enhancing the expression of MKP-1 and ANXA1. MIF enhances cell proliferation, migration, and invasion through the enzymatic site-dependent activation of the ERK1/2 MAPK after endocytosis or interaction with CD74. Both GCs and MIF down-regulate the expression of GR. RU 486 is a GR antagonist, PD 98059 is a specific inhibitor of MEK1/2 phosphorylation, and ISO-1 is a specific inhibitor of the enzymatic site of MIF. EGFR, epidermal growth factor receptor.