The incidence of thyroid cancer in the world is increasing year by year, among which PTC accounts for more than 80%. Iodine is an essential trace element for thyroid hormone synthesis, but the relationship between excessive iodine and thyroid cancer is not clear. This study assumes that high iodine intake is related to the occurrence of thyroid cancer, and may affect the cell cycle through AKT/mTOR signaling pathway and promote the progress of cancer. The human PTC cell line TPC-1 was treated with different concentrations of potassium iodide (KI) to evaluate its effect on cell proliferation and migration. The results showed that an appropriate concentration of KI (such as 10-3 mM) could significantly enhance the proliferation of TPC-1 cells, and a high concentration of KI(≥1 mM) might inhibit cell proliferation. In addition, the expression of key proteins in the AKT/mTOR signaling pathway (such as p-AKT, p-mTOR, p-P706k) was up-regulated in TPC-1 cells treated with high iodine, indicating that the AKT/mTOR signaling pathway was activated. After the AKT/mTOR signaling pathway inhibitor LY294002 was used, the cell proliferation and migration ability decreased significantly, and cell cycle analysis showed that more cells treated with high iodine entered the S phase, while the proportion of cells in the G1 phase increased after LY294002 treatment. To sum up, this study provides preliminary evidence that an appropriate amount of KI affects cell proliferation and migration by activating the AKT/mTOR signaling pathway and inducing Cyclin D1 overexpression, thus promoting the development of PTC cell line TPC-1. This study is of great significance for understanding the relationship between excessive iodine intake and thyroid cancer and developing new prevention and treatment strategies.
