Abstract
High iodine can alter the proliferative activity of thyroid cancer cells, but the underlying mechanism has not been fully elucidated. Here, the role of high iodine in the proliferation of thyroid cancer cells was studied. In this study, we demonstrated that high iodine induced the proliferation of BCPAP and 8305C cells via accelerating cell cycle progression. The transcriptome analysis showed that there were 295 differentially expressed genes (DEGs) in BCPAP and 8305C cells induced by high iodine, among which CDK1 expression associated with the proliferation of thyroid cancer cells induced by high iodine. Moreover, the western blot analysis revealed that cells exposed to high iodine enhanced the phosphorylation activation of AKT and the expression of phospho-Wee1 (Ser642), while decreasing the expression of phospho-CDK1 (Tyr15). Importantly, the inhibition of AKT phosphorylation revered the expression of CDK1 induced by high iodine and arrested the cell cycle in the G1 phase, decreasing the proliferation of thyroid cancer cells induced by high iodine. Taken together, these findings suggested that high iodine induced the proliferation of thyroid cancer cells through AKT-mediated Wee1/CDK1 axis, which provided new insights into the regulation of proliferation of thyroid cancer cells by iodine.
Highlights
Follicular cell-derived thyroid cancer is the most common endocrine cancer, which can be mainly classified into papillary cancer (PTC), follicular cancer (FTC) and anaplastic cancer (ATC) [1]
CCK-8 assays were used to identify the effect of high iodine on the proliferation of BCPAP and 8305C cells
Compared with the control groups, treatment with 2 mmol/L KIO3 for 72 h increased the EdU-positive rate of BCPAP and 8305C cells by 27.5% and 53.4%, respectively. These results indicated that exposure to high iodine promoted the proliferation of BCPAP and 8305C cells
Summary
Follicular cell-derived thyroid cancer is the most common endocrine cancer, which can be mainly classified into papillary cancer (PTC), follicular cancer (FTC) and anaplastic cancer (ATC) [1]. PTC is a well-differentiated carcinoma with an excellent prognosis, and accounts for over 80% of the total incidence [2]; while ATC is the most aggressive thyroid carcinoma with poor prognosis, only accounting for less than 5% of the incidence, but it accounts for a large proportion of the mortality [2,3,4,5]. Iodine Induces Proliferation in TC suspected to be the risk factors, especially the relationship between iodine excess intake and thyroid cancer [13,14,15,16]. It is imminent to explore the implications of high iodine exposure on thyroid cancer
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