长链非编码RNA RP11-436H11.5作为ceRNA调控BCL-W介导的肾癌侵袭转移的分子机制

BCL-W介导肾癌侵袭转移，但其调控机制不清。申请者发现长链非编码RNA RP11-436H11.5在肾癌组织中高表达，并与BCL-W表达正相关；肾癌细胞株中转染RP11-436H11.5沉默质粒后；细胞侵袭转移能力下降，BCL-W表达降低；肾癌细胞中BCL-W是miR-335靶基因之一；理论预测RP11-436H11.5存在与miR-335结合位点，提示RP11-436H11.5可能作为ceRNA调控BCL-W表达及其介导的肾癌侵袭转移。本项目拟分析RP11-436H11.5介导的肾癌细胞侵袭和转移与BCL-W的相关性，明确RP11-436H11.5以ceRNA方式调控BCL-W表达作用机制，考察RP11-436H11.5通过miR-335调节BCL-W对肾癌细胞侵袭和转移的影响，为寻找肾癌侵袭转移形成与逆转的新靶点，进一步阐明肾癌发生发展机制奠定理论与实验基础。

The mechanism of invasion and metastasis of renal cell carcinoma mediated by BCL-W is not clear now. We found that lncRNA RP11-436H11.5 was highly expression in renal cell carcinoma and was positively correlated with the expression of BCL-W. The invasion and metastasis of renal cell carcinoma and the expression of BCL-W decreased when RP11-436H11.5 was transfected by silence plasmid. BCL-W was one of the targeted genes of miR-335 in renal cancer cell. We found that there was a binding site of miR-335 in RP11-436H11.5 by theoretical prediction, suggesting that RP11-436H11.5 could regulate BCL-W expression and influence invasion and metastasis of renal cell carcinoma as a ceRNA. Our project aims to analyze the relationship between invasion and metastasis of renal cell carcinoma mediated by RP11-436H11.5 and BCL-W. We also want to find the mechanism of action of RP11-436H11.5 as a ceRNA regulating BCL-W. Finally, we investigate the invasion and metastasis of renal cell carcinoma by RP11-436H11.5 regulating the activity of BCL-W through miR-335 intervention. The results of this study are expected to find a new target for reversal of invasion and metastasis of renal cell carcinoma. Further more, it could lay a theoretical and experimental foundation for the mechanism of genesis and development of renal cell carcinoma.