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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: J Cell Physiol. 2018 Aug 1;234(3):2822–2836. doi: 10.1002/jcp.27100

FIGURE 4.

FIGURE 4

Effects of inhibition of PP2A by okadaic acid or ectopic expression of dominant negative or wild-type PP2A in Rh1, Rh30 and/or HeLa cells on resveratrol’s inhibition of IGF-1-induced Erk1/2 activation and cell adhesion. Resveratrol inhibits IGF-1-stimulated Erk1/2 activation and cell adhesion via activating PP2A. Serum-starved Rh1 and HeLa cells, pre-treated with/without okadaic acid (100 nM) for 1 h, or serum-starved Rh30 and/or HeLa cells, infected with Ad-GFP (as control), Ad-dn-PP2A and Ad-PP2A, respectively, and then pre-incubated with/without U0126 (5 μM) for 1 h, were treated with/without resveratrol (100 μM) for 4 h, followed by stimulation with/without IGF-1 (10 ng/ml) for 1 h. (a, d, g) Total cell lysates were subjected to Western blotting using indicated antibodies. The blots were probed for β-tubulin as a loading control. Similar results were observed in at least three independent experiments. (b, e, h) The blots for de-PP2A, p-PP2A, and p-Erk1/2 were semi-quantified using NIH image J. (c, f, i) Adherent cells were determined using CN IV-coated cell adhesion assay. Results are presented as mean ± SEM (n = 3–6). a p < 0.05, difference with control group; b p < 0.05, difference with IGF-1 group; c p < 0.05, difference with IGF-1/resveratrol group or IGF-1/okadaic acid group; d p < 0.05, Ad-dn-PP2A group or Ad-PP2A group vs. Ad-GFP group.