Background
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.
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.
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.