碘过量通过调控miR-146b-5p促进甲状腺乳头状癌发生的机制

Iodine intake excess can result in the increase of papillary thyroid carcinoma (PTC) incidence. microRNAs play an important role in regulating gene expression. Studies showed that miR-146b-5p promoted the ocurrence of PTC by regulating the expression of its target gene SMAD4. However, whether iodine intake excess can promot the occurrence of PTC by regulating miR-146b-5p remains unknown. Our previous study showed iodine intake and miR-146b-5p expression correlated positively through analyzing miR-146b-5p expression in PTC tisses of patients from different iodine intake regions. Therefore,we hypothesize that miR-146b-5p expression increase and its regulation on SMAD4 could be new mechanism of PTC occurrence. In this study, we will verify the hypothesis above using the methods including cell transfection, and quantitative PCR. This study could reveal the role of microRNA in iodine excess-induced thyroid papillary carcinoma for the first time, provide new insights into clarifing the molecular mechanism of iodine-induced PTC, and provide theoretical basis for making iodine supplement strategy by the government and the treatment of thyroid associated diseases.

碘摄入过多能够导致甲状腺乳头状癌（Papillary thyroid carcinoma,PTC）的发病率升高。microRNA是一类对基因调控起着重要作用的RNA。研究表明miR-146b-5p能够通过调控其靶基因SMAD4的表达促进PTC的发生。但是，碘摄入过量是否通过调节miR-146b-5p促进PTC的发生目前尚无报导。我们在前期工作通过分析不同碘摄入地区PTC组织中miR-146b-5p表达后发现碘摄入量与miR-146b-5p表达呈正相关。因此,我们推测"miR-146b-5p表达上调及对SMAD4的调节作用"可能是碘过量促进PTC发生的新机制。本研究拟应用细胞转染、定量PCR等实验手段证实上述假说。本研究将首次揭示microRNA在碘诱发甲状腺乳头状癌中的作用，为阐明碘诱发PTC的分子机制提供新思路，从而可能为政府制定科学补碘策略及甲状腺相关疾病的防治提供理论依据。