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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 3. The decrease of NIS protein levels by MEK inhibition is mediated by lysosomal but not proteosomal pathway in MCF-7-tRA/H cells.

Figure 3

A. Western blot analysis showed that proteasome inhibitors did not prevent the decrease of NIS protein levels in U0126 treated MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO or U0126 for 24 hours, along with or without proteasome inhibitors MG132 or β-lactone for 8 hours. β-actin served as a loading control and p53 was included to ensure the efficacy of proteasome inhibition. The results are representative of 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). C. Western blot analysis showed that lysosome inhibitors prevented the decrease of NIS protein levels in U0126 treated MCF-7-tRA/H cells. MCF-7 cells treated with tRA/H were cultured in the presence of DMSO or U0126 for 24 hours, along with or without lysosome inhibitors leupeptin or chloroquine for 8 hours. β-actin served as a loading control. The results are representative of three independent experiments. D. 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).