转移性肾癌对放化疗均不敏感，是目前肾癌治疗中的难点，因此肾癌转移的机制已成为当下研究的焦点。我们前期研究发现：睾丸孤核受体4（TR4）高表达促进肾细胞癌侵袭转移；TR4差异表达肾癌细胞circRNA芯片筛选表明circ_000926在TR4敲低细胞中低表达；体外实验提示circ_000926与肾癌细胞的侵袭转移相关。因此，我们认为TR4可能通过上调circ_000926的表达从而促进肾癌的转移。本课题拟通过一系列体内外实验，综合运用CRISPR、RNA-IP、circRNA敲低与过表达、裸鼠原位肾癌移植模型、双荧光素酶报告基因等技术，从细胞、动物、临床多个层次研究TR4在肾癌转移中的作用，阐明TR4调控circ_000926影响肾癌转移的具体分子机制，为转移性肾癌的诊治提供新的思路和理论依据。

The metastatic renal cell carcinoma (RCC) resists to both radio- and chemo-therapy and has become a major obstacle in the treatment of RCC, thus its metastatic mechanism becomes a research focus of the present study. Our previous work suggest that high expression of the testicular nuclear receptor 4 (TR4) may promote the migration and invasion of RCC. Through circRNA chip screening of TR4 differentially expressed cells, we found that circ_000926 decreased in TR4 knocked-down cells and circ_000926 was involved in RCC metastasis. Thus we speculate that TR4 may promote RCC metastasis through upregulating circ_000926 expression. Our study aims to probe the role of TR4/circ_000926 signaling pathway in migration and invasion of RCC, to explore its possible mechanism from the molecular, cellular, creatural and clinical fields. Insight in to the molecular mechanism of RCC metastasis may provide novel ideas and theoretical basis of therapeutic targets for kidney cancer.