已发表论文

沉默 circZFR 通过调节 miR-206 抑制人肾癌细胞的增殖、迁移和侵袭

 

Authors Wang M, Gao Y, Liu J

Received 8 May 2019

Accepted for publication 27 August 2019

Published 13 September 2019 Volume 2019:12 Pages 7537—7550

DOI https://doi.org/10.2147/OTT.S215012

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Aruna Narula

Peer reviewer comments 2

Editor who approved publication: Dr Sanjay Singh

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.
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




Figure 8 Met was the target of miR-206 in CAKI-1 and...