Pengcheng Sun, Ziqi Wang, Luyao Yin, Xiangwei Zhu, Liang Liu, Yuwei Liu, Lechen Li, Wanhai Xu
Department of Urology, The Fourth Hospital of Harbin Medical University, Harbin 150001, China.
Department of Urology, The Fourth Hospital of Harbin Medical University, Harbin 150001, China
Biosci Rep. 2017 May 19;37(3). doi: 10.1042/BSR20170270. Print 2017 Jun 30.
Abnormal expression of miRNAs contributed to cancers through regulation of proliferation, apoptosis and drug resistance of cancer cells. The present study was designed to investigate the effect of on renal cell carcinoma (RCC) and its possible mechanism. Forty paired clear cell RCC (ccRCC) tissues and adjacent normal kidney tissues were obtained from patients, who were not treated by chemotherapy or radiotherapy. RT-PCR was performed to detect expression of in the ccRCC tissues. Effects of on cell viability, apoptosis, migration and invasion were detected in ACHN cells. Western blotting (WB) was employed to detect the downstream targets of We found that in ccRCC tissues was decreased. We treated ACHN cells with mimics and inhibitors and found that inhibited viability, migration and invasion of ACHN cells. promoted ACHN cells' apoptosis. VEGFR-2 was predicted as a possible target of Luciferase reporter assay proved that suppressed VEGFR-2 directly by binding to its 3'-UTR. Further studies showed that influenced the MEK/ERK and p38 MAPK signalling pathways. Our findings demonstrated that could suppress RCC by targeting VEGFR-2.
微小RNA（miRNAs）的异常表达通过调节癌细胞的增殖、凋亡和耐药性促进癌症发生。本研究旨在探讨[具体内容未给出]对肾细胞癌（RCC）的影响及其可能机制。从未经化疗或放疗的患者中获取40对透明细胞RCC（ccRCC）组织和相邻正常肾组织。采用逆转录-聚合酶链反应（RT-PCR）检测ccRCC组织中[具体内容未给出]的表达。检测[具体内容未给出]对ACHN细胞活力、凋亡、迁移和侵袭的影响。采用蛋白质免疫印迹法（WB）检测[具体内容未给出]的下游靶点。我们发现ccRCC组织中[具体内容未给出]表达降低。用[具体内容未给出]模拟物和抑制剂处理ACHN细胞，发现[具体内容未给出]抑制ACHN细胞的活力、迁移和侵袭。[具体内容未给出]促进ACHN细胞凋亡。血管内皮生长因子受体2（VEGFR-2）被预测为[具体内容未给出]的一个可能靶点。荧光素酶报告基因检测证明[具体内容未给出]通过与VEGFR-2的3'-非翻译区（3'-UTR）结合直接抑制VEGFR-2。进一步研究表明[具体内容未给出]影响丝裂原活化蛋白激酶/细胞外信号调节激酶（MEK/ERK）和p38丝裂原活化蛋白激酶（p38 MAPK）信号通路。我们的研究结果表明[具体内容未给出]可通过靶向VEGFR-2抑制RCC。
