Renal cell carcinoma (RCC) is the seventh most common site for malignant tumours worldwide leading to a high risk of death. NKAP is a conserved nuclear protein that has critical roles in the development, maturation, and functional acquisition of T cells, iNKT cells, and cancers. But the function and underlying mechanism of NKAP in RCC is still unknown. Knockdown of NKAP by siRNA interference (siNKAP) was used to explore the roles of NAKP in human RCC cells. Here, we found that siNKAP strongly inhibited the proliferation and motility of Ketr‐3 and 786‐0 cells and induced cell apoptosis. Furthermore, the expression of anti‐apoptotic protein Bcl2 in the siNKAP group was strongly decreased, while the expression of pro‐apoptotic proteins Bax, cleaved Caspase‐3, and cleaved Caspase‐9 was significantly increased. Finally, to identify the potential mechanisms, we detected related proteins of the AKT/mTOR signalling pathway by western blot assay. We found that siNKAP significantly inhibited the expression of cyclin D1 and the phosphorylation of AKT and mTOR. The findings for the first time reveal that the AKT/mTOR signalling pathway is involved in the oncogenic role of NKAP in RCC, which provides an important basis for exploring the molecular regulation mechanism of RCC.

中文翻译：

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NKAP通过AKT / mTOR信号通路促进肾细胞癌的生长。

肾细胞癌（RCC）是全世界导致高死亡风险的第七大最常见恶性肿瘤部位。NKAP是一种保守的核蛋白，在T细胞，iNKT细胞和癌症的发育，成熟和功能获得中具有关键作用。但NKAP在RCC中的功能和潜在机制尚不清楚。siRNA干扰（siNKAP）NKNK的敲低被用来探索NAKP在人类RCC细胞中的作用。在这里，我们发现siNKAP强烈抑制Ketr-3和786-0细胞的增殖和运动并诱导细胞凋亡。此外，siNKAP组中抗凋亡蛋白Bcl2的表达显着降低，而凋亡前蛋白Bax，裂解的Caspase-3和裂解的Caspase-9的表达显着增加。最后，为了确定潜在的机制，我们通过蛋白质印迹分析检测了AKT / mTOR信号通路的相关蛋白。我们发现siNKAP显着抑制细胞周期蛋白D1的表达以及AKT和mTOR的磷酸化。首次发现，AKT / mTOR信号通路参与了NKAP在RCC中的致癌作用，为探索RCC的分子调控机制提供了重要依据。