Se-Methylselenocysteine inhibits proliferation and migration of anaplastic thyroid carcinoma cells through the ROS-ERK1/2 signaling pathway

Abstract Se-Methylselenocysteine (MSC) is a major organic selenium compound that possesses anticancer activity. However, the antitumor effect of MSC in anaplastic thyroid carcinoma (ATC) remains to be investigated. In this study, the two human ATC cell lines 8305 and BHT101 were used to examine the potential antitumor effect of MSC in ATC. Cell viability was measured using Cell Counting Kit-8, and the migration ability of the cells was evaluated by Transwell assays. The 2,7-dichlorodihydrofluorescein diacetate(DCFH-DA) was used to analyze reactive oxygen species production. Changes in extracellular regulated-protein kinases 1/2 (ERK1/2) and phosphorylation level of ERK1/2 proteins were analyzed by western blotting in 8505C and BHT101 cells. The results indicated that MSC dose-dependently inhibited proliferation and migration of ATC cells.MSC also decreased the phosphorylation level of ERK1/2 and increased intracellular reactive oxygen species (ROS ) level in ATC cells.The inhibitory effect of MSC on ERK1/2 signaling was reversed by a ROS scavenger.In conclusion, MSC exerted its antitumor activity in ATC cells by inhibiting ERK1/2 signaling via a ROS-dependent pathway. Therefore, our results suggested that MSC had potential clinical value in the treatment of ATC.