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. Author manuscript; available in PMC: 2013 Nov 22.
Published in final edited form as: Endocr Relat Cancer. 2013 Mar 22;20(2):10.1530/ERC-12-0342. doi: 10.1530/ERC-12-0342

Figure 1. MEK inhibition decreases NIS protein levels and NIS-mediated RA radioactive iodide uptake in tRA/H-treated MCF-7 human breast cancer cells.

Figure 1

(A) Western blot analysis showed that MEK inhibitor U0126 (left panel) or recombinant adenovirus carrying dominant negative MEK1 A217/A221 (right panel) decreased NIS protein levels in MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO, U0126, or inactive analog U0124 for 24 hours, or were infected with recombinant adenovirus carrying LacZ (rAdLacZ) or dominant negative MEK1 (rAdDNMEK1) at a multiplicity of infection (MOI) of 5 for 24 hours prior to western blot analysis. β-actin served as a loading control. The results are representative of at least two independent experiments. (B) Bar graph indicates the densitometry values of NIS protein level normalized with β-actin of cells under various treatments (represented as percentage relative to MCF-7/tRA/H or MCF-7/tRA/H/Lac-Z control). (C) U0126 decreased radioactive iodide uptake in a dose-dependent manner in tRA/H-induced MCF-7 cells. The results are representative of three independent experiments performed in triplicate and the mean ± SD are shown. Asterisk indicates statistically significant difference (P< 0.05). Parallel iodide uptake experiments were conducted in the presence of perchlorate NIS inhibitor to examine RAIU activity not contributed by NIS-mediated iodide uptake.