Se-methylselenocysteine Inhibits Migration and Glycolysis in Anaplastic Thyroid Carcinoma Cells via the ERK1/2 Signaling Pathway in vitro

Objective. The aim of the present study was to determine the effects of selenium-methylselenocysteine (MSC) on the viability, migration, and glycolysis of human ATC cell lines 8305 and BHT101 in vitro. Methods. Cells were treated with MSC and viability was determined using the Cell Counting Kit 8 assay. The migratory ability of cells was detected using aTranswell migration assay, and the expression levels of proteins involved in the ERK1/2, JNK, and p38 signaling pathways were measured by western blotting. Glycolysis was investigated by determining glucose consumption, lactate production, and protein levels of key glycolytic enzymes (glucose transporter 1, hexokinase 2, and lactate dehydrogenase A). Results. MSC inhibited the viability, migration, and glycolysis of ATC cells. Phosphorylated (p)-ERK1/2 expression decreased with increasing MSC concentration; however, p-JNK and p-p38 levels were unaffected in cell lines 8305C and BHT101. Epidermal growth factor induced activation of ERK1/2 and impaired the inhibitory effect of MSC on ATC cell viability, migration, and glycolysis. Conclusions. These findings indicated that MSC inhibited the viability, migration, and glycolysis of ATC cells via the ERK1/2 signaling pathway, suggesting that MSC may represent a novel therapeutic agent for ATC.