Rosiglitazone Inhibits Adrenocortical Cancer Cell Proliferation by Interfering with the IGF-IR Intracellular Signaling
Figure 7
ERK and Akt activation downstream
of the IGF-IR mediates IGF-I stimulation of cell proliferation. Western
blot analysis of H295R cell lysates following 15-minute stimulation with 10 nM
IGF-I in the presence or absence of 1 M NVP-AEW541 (NVP) inhibitor of the tyrosine
kinase activity of IGF-IR (a). The inhibitor blocks phosphorylation of Akt
(upper panel) and of ERK1/2 (middle panel) both in basal conditions and
following IGF-I stimulation. Lane protein normalization for actin is shown in
the lower panel. Molecular weight markers are indicated. Cell
proliferation was evaluated by MTS assay following 2 or 4 day stimulation with
the indicated treatments (10 nM IGF-I, 20 M RGZ, 1 M NVP) in SW13 (b) or H295R (c) cells,
respectively. Mean SE
percentage of OD over respective control IGF-I taken as 100%. # versus IGF-I, n = 6.
