Background/Aim: MEK-ERK pathway plays major roles in the progression of thyroid cancer, while the use of MEK-ERK inhibitors has been limited by its toxicity. We investigated the effect of sodium selenite as an adjunct for MEK-ERK inhibitors to avoid the toxicity of ERK inhibitors. Materials and Methods: TPC1, 8505C and HTori-3 cells were treated with U0126 (MEK-ERK inhibitor) and cell viability was counted in the Neubauer chamber. The synergistic effects of sodium selenite and U0126 were also measured. The expression of ERK, p-ERK, and p90RSK was determined by western blot. Results: Treatment with U0126 inhibited proliferation of TPC1 and 8505C cells in a dose-dependent manner. When 5 μM sodium selenite was added to 1 μM U0126, relative cell survival further decreased. Decreased expression of p90RSK indicated that sodium selenite down-regulated ERK signaling in thyroid cancer cells. Conclusion: The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition.
Bibliographical noteFunding Information:
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science & ICT (2017R1C1B5076977) and the Ewha Womans University Research Grant of 2017.
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- ERK pathway
- MEK-ERK inhibitor
- Thyroid cancer