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
Conclusion
The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition.
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.