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Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206
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 ne...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6750881/ https://www.ncbi.nlm.nih.gov/pubmed/31571906 http://dx.doi.org/10.2147/OTT.S215012 |
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author | Wang, Mi Gao, Yisheng Liu, Jie |
author_facet | Wang, Mi Gao, Yisheng Liu, Jie |
author_sort | Wang, Mi |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6750881 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-67508812019-09-30 Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 Wang, Mi Gao, Yisheng Liu, Jie Onco Targets Ther Original Research 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. Dove 2019-09-13 /pmc/articles/PMC6750881/ /pubmed/31571906 http://dx.doi.org/10.2147/OTT.S215012 Text en © 2019 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wang, Mi Gao, Yisheng Liu, Jie Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title | Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title_full | Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title_fullStr | Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title_full_unstemmed | Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title_short | Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206 |
title_sort | silencing circzfr inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating mir-206 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6750881/ https://www.ncbi.nlm.nih.gov/pubmed/31571906 http://dx.doi.org/10.2147/OTT.S215012 |
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