中文摘要：

是的 MicroRNAs (miRNAs ) 功能在各种各样的癌症的基因表示的关键管理者。在这研究，目的是在 neuroblastoma (NB ) 探索角色和 miR-181c 的规定机制房间。我们发现 miR-181c 是在变形 NB 纸巾的 downregulated，与主要 NB 纸巾相比。当 miR-181c 抑制增加了房间增长，移植，和侵略时，然后功能的研究显示 miR-181c overexpression 禁止了 NB 房间增长，移植，和侵略。EGFP 记者试金，即时聚合酶链反应和西方的污点分析验证了那 Smad7 是 miR-181c 的一个直接目标。MiR-181c 在 mRNA 和蛋白质层次减少了 Smad7 表示。最后，功能的试金证明在房间上击倒的 Smad7 的效果类似于 miR-181c overexpression 的。重要地， Smad7 overexpression 能恢复被 miR-181c 导致的 antitumor 效果。在结论，我们的结果证明 miR-181c 通过 Smad7 的抑制禁止 NB 房间生长和转移相关的特点，作为肿瘤 suppressor 工作。而且，我们的结果建议 miR-181c 可以为 NB 病人用作一个重要治疗学的目标。

英文摘要：

MicroRNAs （miRNAs） function as key regulators of gene expression in various cancers. In this study, the aim is to explore the roles and regulation mechanism of miR-181c in neuroblastoma （NB） cells. We found that miR-181c was downregulated in metastatic NB tissues, compared with primary NB tissues. Then functional studies indicated that miR-181 c overexpression inhibited NB cell proliferation, migration, and invasion, while miR-181c inhibition increased cell proliferation, migration, and invasion. EGFP reporter assay, real-time polymerase chain reaction and western blot analysis validated that Smad7 was a direct target of miR- 181c. MiR-181c reduced Smad7 expression at both mRNA and protein levels. Finally, functional assays showed that the effect of Smad7 knockdown on cells was similar to that of miR-181c overexpression. Importantly, Smad7 overexpression could restore the antitumor effects that were induced by miR-181 c. In conclusion, our results demonstrated that miR- 181c inhibits NB cell growth and metastasis-related traits through the suppression of SmadT, functioning as a tumor suppressor. Moreover, our results suggested that miR-181c may serve as an important therapeutic target for NB patients.