Wang Mi, Gao Yisheng, Liu Jie
Department of Urology, The Second Affiliated Hospital, University of South China, Hengyang 421000, Hunan, People's Republic of China.
Department of Urology, Linyi People's Hospital, Linyi 276003, Shandong, People's Republic of China.
Onco Targets Ther. 2019 Sep 13;12:7537-7550. doi: 10.2147/OTT.S215012. eCollection 2019.
Renal cell carcinoma (RCC) is the most prevalent kind of kidney cancer. At present, the most efficient treatment mean is surgery. 40% patients with clear cell RCC (ccRCC) relapse after surgery. Identifying novel therapeutic markers and spots for early detection and treatment of RCC is necessary.
qRT-PCR was utilized to quantify circZFR and miR-206 expression in CAKI-1 and ACHN cells. Cell viability was detected by CCK-8 assay. Colony formation capacity was measured by colony formation assay. Transwell assay was utilized to investigate migration and invasion capacity. Expression of migration and apoptosis-associated proteins was quantified by Western blot.
As a result, circZFR was highly expressed in RCC tissues and cells. Si-circZFR suppressed cell growth, migration and invasion of experimental cells. In addition, knockdown of circZFR upregulated miR-206 expression. Moreover, the antigrowth, antimigrating and anti-invasive effects of si-circZFR were attenuated when downregulating miR-206. Furthermore, Met is the target gene of miR-206 in experimental cells. The suppression on these signaling pathways was acted by targeting miR-206/Met axis.
The results demonstrated si-circZFR inhibited cell growth, migration and invasion in experimental cells by up-regulating of miR-206. Furthermore, si-circZFR suppressed Wnt/β-catenin and PI3K/AKT pathways via targeting miR-206/Met axis.
肾细胞癌(RCC)是最常见的肾癌类型。目前,最有效的治疗方法是手术。40%的透明细胞肾细胞癌(ccRCC)患者术后会复发。因此,有必要寻找新的治疗标志物以及早期检测和治疗RCC的靶点。
采用qRT-PCR法检测CAKI-1和ACHN细胞中circZFR和miR-206的表达。通过CCK-8法检测细胞活力。采用集落形成试验检测集落形成能力。利用Transwell试验研究细胞迁移和侵袭能力。通过蛋白质印迹法检测迁移和凋亡相关蛋白的表达。
circZFR在RCC组织和细胞中高表达。Si-circZFR抑制实验细胞的生长、迁移和侵袭。此外,敲低circZFR可上调miR-206的表达。而且,下调miR-206可减弱si-circZFR的抗生长、抗迁移和抗侵袭作用。此外,Met是实验细胞中miR-206的靶基因。通过靶向miR-206/Met轴可抑制这些信号通路。
结果表明,si-circZFR通过上调miR-206抑制实验细胞的生长、迁移和侵袭。此外,si-circZFR通过靶向miR-206/Met轴抑制Wnt/β-连环蛋白和PI3K/AKT信号通路。