Identification of new therapeutic target molecules for renal cell carcinoma

近年来，肾细胞癌患者数量呈上升趋势。尽管抗血管内皮生长因子治疗改善了这些患者的预后，但大多数肿瘤获得耐药性并最终进展。已有研究表明，VHL基因在70%的肾细胞癌中发生突变，且聚集素受pVHL调控。有人认为，聚集素具有肿瘤抑制功能，因为该分子被pVHL下调。在此基础上，我们克隆了聚集素的启动子区域，以研究该蛋白的调控机制以及寻找新的肾癌治疗靶点。因此，MAP2K1被确定为肾癌新的分子治疗靶点。

Recently, the number of RCC patients is increasing. Although, anti-VEGF therapies improve the prognosis of those patients, most of tumors acquire resistance and finally progress. It has been reported that VHL gene is mutated in 70% of RCC and we showed that clusterin was regulated by pVHL. It was suggested clusterin had a tumor suppressor function since this molecule is down regulated by pVHL. Based on these, we have cloned the promoter region of clusterin to examine the regulation mechanisms of the protein as well as the identification of new therapeutic target for RCC. As a result of this, MAP2K1 was identified as new molecular therapeutic target for RCC.