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Background: Excess iodine inhibits thyroid follicular cell proliferation associated with TGFβ pathway activation, although thyroid cancers are frequently refractory to TGFβ signaling. The TGFβ pathway is predicted to be regulated by miR-17-92 cluster microRNAs. MicroRNAs are small noncoding RNAs that inhibit target mRNA translation and have emerged as potent modulators of tumorigenesis. Although the BRAF^V600E mutation is the most prevalent alteration in thyroid cancer, the impact of iodine intake on BRAF-mediated oncogenesis remains unclear. Therefore, the aim of this study was to investigate the influence of high iodine on miR-17-92 transcriptional regulation and expression in thyroid cells expressing activated BRAF.

Methods: Rat thyroid follicular cells that conditionally express BRAF^V600E under doxycycline stimulation (PC-BRAF^V600E-6) were derived from the PCCl3 line. These cells were treated …