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Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7
Renal cell carcinoma (RCC) is the most common type of kidney cancer whose incidence has gradually increased worldwide. MicroRNAs (miRNAs) represent a type of short endogenous non-coding RNA containing approximately 22 nucleotides, which are capable of regulating mRNAs at the post-transcriptional lev...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074420/ https://www.ncbi.nlm.nih.gov/pubmed/32256821 http://dx.doi.org/10.3892/ol.2020.11443 |
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author | Zeng, Rong Huang, Jing Sun, Yujie Luo, Juan |
author_facet | Zeng, Rong Huang, Jing Sun, Yujie Luo, Juan |
author_sort | Zeng, Rong |
collection | PubMed |
description | Renal cell carcinoma (RCC) is the most common type of kidney cancer whose incidence has gradually increased worldwide. MicroRNAs (miRNAs) represent a type of short endogenous non-coding RNA containing approximately 22 nucleotides, which are capable of regulating mRNAs at the post-transcriptional level in human cells. miRNAs have been demonstrated to mediate gene expression by influencing important regulatory genes. Accumulating evidence indicates that certain miRNAs are involved in RCC development. The present study investigated the underlying mechanism and functional role of miR-92a-3p in RCC cells using reverse transcription-quantitative polymerase chain reaction, western blotting, 3′ UTR luciferase assay, cell proliferation assay and soft agar assay. The results demonstrated that miR-92a-3p expression level is significantly upregulated in RCC tissues and cell lines; however, F-box and WD repeat domain containing 7 (FBXW7) expression level was significantly downregulated in RCC tissues and cell lines. Subsequently, whether FBXW7 could be considered as a direct target of miR-92a-3p in RCC cells was investigated. The results demonstrated that miR-92a-3p overexpression significantly promoted RCC cell proliferation and colony formation. Conversely, miR-92a-3p downregulation significantly inhibited RCC cell proliferation and colony formation. In addition, FBXW7 knockdown significantly enhanced RCC cell proliferation and colony formation. Conversely, FBXW7 overexpression significantly inhibited RCC cell proliferation and colony formation. Collectively, these results demonstrated that miR-92a-3p/FBXW7 pathway may represent a novel strategy and therapeutic target for RCC. |
format | Online Article Text |
id | pubmed-7074420 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-70744202020-03-31 Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 Zeng, Rong Huang, Jing Sun, Yujie Luo, Juan Oncol Lett Articles Renal cell carcinoma (RCC) is the most common type of kidney cancer whose incidence has gradually increased worldwide. MicroRNAs (miRNAs) represent a type of short endogenous non-coding RNA containing approximately 22 nucleotides, which are capable of regulating mRNAs at the post-transcriptional level in human cells. miRNAs have been demonstrated to mediate gene expression by influencing important regulatory genes. Accumulating evidence indicates that certain miRNAs are involved in RCC development. The present study investigated the underlying mechanism and functional role of miR-92a-3p in RCC cells using reverse transcription-quantitative polymerase chain reaction, western blotting, 3′ UTR luciferase assay, cell proliferation assay and soft agar assay. The results demonstrated that miR-92a-3p expression level is significantly upregulated in RCC tissues and cell lines; however, F-box and WD repeat domain containing 7 (FBXW7) expression level was significantly downregulated in RCC tissues and cell lines. Subsequently, whether FBXW7 could be considered as a direct target of miR-92a-3p in RCC cells was investigated. The results demonstrated that miR-92a-3p overexpression significantly promoted RCC cell proliferation and colony formation. Conversely, miR-92a-3p downregulation significantly inhibited RCC cell proliferation and colony formation. In addition, FBXW7 knockdown significantly enhanced RCC cell proliferation and colony formation. Conversely, FBXW7 overexpression significantly inhibited RCC cell proliferation and colony formation. Collectively, these results demonstrated that miR-92a-3p/FBXW7 pathway may represent a novel strategy and therapeutic target for RCC. D.A. Spandidos 2020-04 2020-03-03 /pmc/articles/PMC7074420/ /pubmed/32256821 http://dx.doi.org/10.3892/ol.2020.11443 Text en Copyright: © Zeng et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zeng, Rong Huang, Jing Sun, Yujie Luo, Juan Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title | Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title_full | Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title_fullStr | Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title_full_unstemmed | Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title_short | Cell proliferation is induced in renal cell carcinoma through miR-92a-3p upregulation by targeting FBXW7 |
title_sort | cell proliferation is induced in renal cell carcinoma through mir-92a-3p upregulation by targeting fbxw7 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074420/ https://www.ncbi.nlm.nih.gov/pubmed/32256821 http://dx.doi.org/10.3892/ol.2020.11443 |
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