乳头状甲状腺癌（PTC)术后行131I内放射是其首选治疗，但25%～50%以上病人出现放射性碘耐受（RAIR）。目前PTC发生RAIR机制尚不清楚。申请人前期实验通过血清microRNA芯片对PTC患者发生RAIR的前后血清中miRs表达变化进行筛查，发现miR-107表达异常增高，干扰miR-107表达能显著提高碘处理蛋白的表达，并确定了miR-107的靶基因TDG。Bio-Plex液相悬浮芯片技术发现RAIR-PTC中TDG表达下调，碘处理相关蛋白表达下降。据此提出假说：RAIR-PTC中异常高表达的miR-107可导致TDG表达下调，导致其与转录因子和转录共激活因子的相互作用受阻，甲状腺特异因子以及甲状腺碘代谢基因去甲基化，及甲状腺信号通路的异常激活等。我们拟通过miR-107功能性获得或缺失系统探讨miR-107调控TDG参与RAIR的发生机制。

131I ablation for removing residual lesion after surgery is the primary therapy for patients who suffer from papillary thyroid cancer. Some 25%~50% of PTC will become radioactive iodine resistant/refractory (RAIR). The mechanisms however, remain largely to be elucidated. The previously work performed by appliciant with serum miRNA array have found that miR-107 was significant higher in 3 PTC patients after RAIR appeared, interfering the miR-107 expression can downregulate the iodine handling proteins expression. Further work have uncovered TDG as a new putative target of miR-107. We also found that the TDG has lower expression in the tissue samples derived from RAIR-PTC patients through Bioplex luminary chip, and the iodine handling proteins were expressed lower among these patients’ samples. Therefore we proposed a hypothesis that miR-107 would be involved in RAIR-PTC by targeting TDG and affecting 131I uptake and iodine handling proteins, TDG may modulate the demethylation of iodine-handling protein, minewhile it can also interact with thryoid specific factor, transcriptional factor or trans-coactivator to affect the signal pathway in thyroid cancer. We want to construct miR-107 overexpression and downregulation models as well as 131I-tolerant PTC cell lines to systemetic investigate the effect of miR-107 on 131I uptake and iodine-handling proteins to further address the mechanisms of miR-107 regulating TDG involve in RAIR-DTC.