肾透明细胞癌（KIRC）的侵袭转移是肾癌致死的最主要原因，但其机制目前仍然不明。我们前期发现STAM在KIRC组织显著下调，且与KIRC恶性程度和预后显著相关，细胞实验结果也显示过表达STAM可显著抑制KIRC细胞的增殖、侵袭和迁移能力，提示STAM可能参与了肾癌发生和进展的调控，但其具体作用与机制仍不清楚。我们通过数据库信息挖掘分析发现lncRNA MAGI2-AS3/miR-142-3p可能是调控STAM表达的关键信号轴，且与KIRC预后密切相关，推测MAGI2-AS3可能通过竞争性抑制miR-142-3p对STAM表达的调控从而抑制了KIRC的侵袭转移，但其具体作用及机制仍需进一步验证研究。本项目拟在前期研究基础上，通过体外细胞和体内移植瘤模型证实并揭示MAGI2-AS3/miR-142-3p靶向STAM调控KIRC侵袭转移的具体作用及分子机制，从而为KIRC的治疗提供新的干预策略。

The invasion and metastasis of kidney clear cell renal carcinoma (KIRC) is the leading cause of death caused by renal cell carcinoma, but its exactly mechanism is still unclear. Our previous microarray analyses found that the expression of STAM (Signal Transducing Adaptor Molecule) in KIRC tissues was significantly decreased, and it was also significantly associated with the malignancy degree and prognosis of KIRC. The results of cell experiment also demonstrated that the proliferation, invasion and metastasis of KIRC cells were significantly inhibited by overexpressing STAM. Thus, our study indicated that STAM may play an important role in regulating the genesis and progression of KIRC, but its specific role and mechanism remain unclear. Our database information mining and analyses found that lncRNA MAGI2-AS3/miR-142-3p may be the key signal axis in regulating the expression of STAM, and they were both significantly associated with the prognosis of KIRC. We hypothesized that MAGI2-AS3 may regulate the expression of STAM by competing inhibit miR-142-3p, and then regulate the invasion and metastasis of KIRC, but further studies are still needed to validate their specific roles and mechanisms. This project intends to clarify the role of lncRNA MAGI2-AS3/miR-142-3p signal regulates the invasion and metastasis of KIRC via targeting STAM and its mechanism through in vitro cell experiment and in vivo xenograft model based on our previous studies, providing a new intervention strategies for the treatment of KIRC.