Abstract
BACKGROUND: Differentiated thyroid cancer (DTC) is the most common thyroid tumor, and the cells of DTC patients can lose the ability to differentiate in their natural state or during treatment and develop radioiodine-refractory DTC (RAI-R DTC), resulting in increased malignancy. Monocarboxylate transporter-1 (MCT(1) ) is positively correlated with the level of malignant of various tumors, and its expression in RAI-R DTC cells is correlated with their biological cell traits. METHODS: Data from 14 iodine-refractory thyroid carcinoma patients were collected, and the effective radioiodine treatment group was used as the control group. The expression of MCT(1) in iodine-refractory thyroid carcinoma and its effect on biological behaviors was observed and the molecular mechanism underlying RAI-R DTC was investigated to determine the cause of the loss of sensitivity of DTC to radioactive iodine using Immunohistochemical staining, Western blot, transwell assay, wound healing assay, flow cytogram assay. RESULTS: Compared to radioiodine-sensitive DTC (RAI-DTC), which was responded to iodine treatment, MCT(1) was highly expressed in RAI-R DTC cells. The overexpression or inhibition of MCT(1) altered the biological characteristics of papillary thyroid carcinoma (TPC-1) cells. The overexpression of MCT(1) in TPC-1 cells increased the invasive, proliferative, and migratory abilities of the cells. Conversely, the downregulation of MCT(1) decreased the invasive, proliferative and migratory abilities of the cells. CONCLUSIONS: The expression of MCT(1) was enhanced in RAI-R DTC cells. MCT(1) appears to be closely related to the invasive metastasis of RAI-R DTC cells, and it may be the cause of the loss of the iodine uptake ability of RAI-R DTC.