Department of Nephrology, Beijing Friendship Hospital, Faculty of Kidney Diseases, Capital Medical University, Beijing, China.
Eur Rev Med Pharmacol Sci. 2020 May;24(9):4738-4744. doi: 10.26355/eurrev_202005_21162.
In recent years, the death number of renal cell carcinoma (RCC) has been enhanced annually. The crucial function of long non-coding RNA (lncRNA) in the occurrence and progression of cancer is of great significance. However, the specific role of lncRNAs in the pathogenesis and prognosis of RCC has not been fully elucidated. Therefore, the aim of this study was to uncover the role of lncRNA RP11-567G11.1 in regulating the progression of RCC.
Relative expression level of RP11-567G11.1 in RCC tissues and cells was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The influences of RP11-567G11.1 on proliferative and invasive abilities of RCC cells were assessed. Subsequently, regulatory effects of RP11-567G11.1 on the viability and apoptosis of DDP-induced RCC cells were examined. Furthermore, the mRNA and protein levels of Notch pathway-related genes Jagged1/HES5/HEY1 in RCC were detected by qRT-PCR and Western blot, respectively.
RP11-567G11.1 expression was significantly up-regulated in RCC tissues and cells. Meanwhile, RP11-567G11.1 was highly expressed in RCC patients with advanced stage. Knockdown of RP11-567G11.1 significantly attenuated proliferative and invasive abilities of 786-O and 769-P cells. Silence of RP11-567G11.1 attenuated viability, while it induced apoptosis in DDP-induced RCC cells. In addition, knockdown of RP11-567G11.1 remarkably down-regulated both mRNA and protein levels of Jagged1, HES5, and HEY1 in RCC.
RP11-567G11.1 accelerates the proliferative and invasive abilities of RCC through activating the Notch pathway. Our findings suggest that it may be a new therapeutic target for RCC.
近年来，肾细胞癌（RCC）的死亡人数逐年增加。长链非编码 RNA（lncRNA）在癌症发生和发展中的关键作用具有重要意义。然而，lncRNAs 在 RCC 发病机制和预后中的具体作用尚未完全阐明。因此，本研究旨在揭示 lncRNA RP11-567G11.1 在调节 RCC 进展中的作用。
采用实时定量聚合酶链反应（qRT-PCR）检测 RCC 组织和细胞中 RP11-567G11.1 的相对表达水平。评估 RP11-567G11.1 对 RCC 细胞增殖和侵袭能力的影响。随后，检测 RP11-567G11.1 对 DDP 诱导的 RCC 细胞活力和凋亡的调节作用。此外，采用 qRT-PCR 和 Western blot 分别检测 RCC 中 Notch 通路相关基因 Jagged1/HES5/HEY1 的 mRNA 和蛋白水平。
RP11-567G11.1 在 RCC 组织和细胞中表达明显上调。同时，在晚期 RCC 患者中 RP11-567G11.1 表达较高。敲低 RP11-567G11.1 显著减弱 786-O 和 769-P 细胞的增殖和侵袭能力。沉默 RP11-567G11.1 减弱 DDP 诱导的 RCC 细胞活力，诱导其凋亡。此外，敲低 RP11-567G11.1 可显著下调 RCC 中 Jagged1、HES5 和 HEY1 的 mRNA 和蛋白水平。
RP11-567G11.1 通过激活 Notch 通路加速 RCC 的增殖和侵袭能力。我们的研究结果表明，它可能成为 RCC 的新治疗靶点。
