| Summary: | Mi Wang,1 Yisheng Gao,2 Jie Liu2 1Department of Urology, The Second Affiliated Hospital, University of South China, Hengyang 421000, Hunan, People’s Republic of China; 2Department of Urology, Linyi People’s Hospital, Linyi 276003, Shandong, People’s Republic of ChinaCorrespondence: Jie LiuDepartment of Urology, Linyi People’s Hospital, No.27 East Section of Jiefang Road, Lanshan District, Linyi 276003, Shandong, People’s Republic of ChinaEmail liu80lj@sina.comBackground: 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.Methods: 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.Results: 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.Conclusion: 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.Keywords: circZFR, miR-206, renal carcinoma cells
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