Sodium Selenite Enhanced the Anti-proliferative Effect of MEK-ERK Inhibitor in Thyroid Cancer Cells

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. TPC1, 8505C and HTori-3 cells were...

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Bibliographic Details
Published in:In vivo (Athens) 2020-01, Vol.34 (1), p.185-190
Main Authors: Kim, Jong Bin, Yang, Eun Yeol, Woo, Joohyun, Kwon, Hyungju, Lim, Woosung, Moon, Byung-In
Format: Article
Language:English
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Summary: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. 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 p90 was determined by western blot. 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 p90 indicated that sodium selenite down-regulated ERK signaling in thyroid cancer cells. The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition.
ISSN:0258-851X
1791-7549
DOI:10.21873/invivo.11760