In the present study we investigated the expression and the functional role of mechanosensitive polycystins in renal cell carcinoma (RCC). In 115 RCC patients we evaluated the protein expression of polycystin-1 (PC1), polycystin-2 (PC2), VEGF and protein components of the PI3K/Akt/mTOR pathway, which have been implicated both in RCC and polycystic kidney disease. PC1 and PC2 demonstrated reduced expression throughout the RCC tissue compared to the adjacent normal tissue. PC1 and PC2 revealed high expression when they were associated with higher grade and decreased 5-year survival respectively. PC1 and PC2 were positively correlated with p110γ subunit of PI3K and high PC1 expressing cells tended to display activation/phosphorylation of Akt. There was also a positive association between PC1 and VEGF expression, whereas PC1 augmented the tumor's microvascular network in stage IV carcinomas. In human RCC cells, functional inhibition of PC1 resulted in upregulation of the PI3K/Akt/mTOR pathway, enhanced cell proliferation and led to inhibition of cell migration. Conclusively, aberrant PC1 regulation is associated with increased angiogenesis and features of advanced disease in RCC tissues.

在本研究中，我们调查了机械敏感性多囊藻毒素在肾细胞癌（RCC）中的表达及其功能。在115位RCC患者中，我们评估了polycystin-1（PC1），polycystin-2（PC2），VEGF的蛋白表达和PI3K / Akt / mTOR通路的蛋白成分，这些蛋白均与RCC和多囊性肾脏疾病有关。与相邻的正常组织相比，PC1和PC2在整个RCC组织中表达降低。PC1和PC2分别与较高的等级和降低的5年生存率相关时显示高表达。PC1和PC2与PI3K的p110γ亚基呈正相关，高表达PC1的细胞倾向于显示Akt的激活/磷酸化。PC1和VEGF表达之间也呈正相关，而PC1增强了肿瘤的表达。IV期癌的微血管网络。在人类RCC细胞中，对PC1的功能抑制导致PI3K / Akt / mTOR通路的上调，增强细胞增殖并导致细胞迁移受到抑制。结论是，异常的PC1调节与RCC组织中血管生成的增强和晚期疾病的特征有关。