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Iodine-131 ( 131 I) is widely used for the treatment of thyroid-related diseases. This study aimed to investigate the expression of  p53  and  BTG2  genes following  131 I therapy in thyroid cancer cell line SW579 and the possible underlying mechanism. SW579 human thyroid squamous carcinoma cells were cultured and treated with  131 I. They were then assessed for  131 I uptake, cell viability, apoptosis, cell cycle arrest, p53 expression, and  BTG2  gene expression. SW579 cells were transfected with BTG2 siRNA, p53 siRNA and siNC and were then examined for the same aforementioned parameters. When treated with a JNK inhibitor of SP600125 and  131 I or with a NF-κB inhibitor of BMS-345541 and  131 I, non-transfected SW579 cells were assessed in JNK/NFκB pathways. It was observed that  131 I significantly inhibited cell proliferation, promoted cell apoptosis and cell cycle arrest. Both BTG2 and p53 expression were enhanced in a dose-dependent manner. An increase in cell viability by up-regulation in  Bcl2  gene, a decrease in apoptosis by enhanced  CDK2  gene expression and a decrease in cell cycle arrest at G 0 /G 1  phase were also observed in SW579 cell lines transfected with silenced  BTG2  gene. When treated with SP600125 and  131 I, the non-transfected SW579 cell lines significantly inhibited JNK pathway, NF-κB pathway and the expression of BTG2. However, when treated with BMS-345541 and  131 I, only the NF-κB pathway was suppressed.  131 I suppressed cell proliferation, induced cell apoptosis, and promoted cell cycle arrest of thyroid cancer cells by up-regulating B-cell translocation gene 2-mediated activation of JNK/NF-κB pathways.

brazilian journal of medical and biological research

Iodine-131 treatment of thyroid cancer cells leads to suppression of cell proliferation followed by induction of cell apoptosis and cell cycle arrest by regulation of B-cell translocation gene 2-mediated JNK/NF-κB pathways