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Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a
MicroRNA-155 (miR-155) is overexpressed in numerous human cancer types and has an oncogenic role. Previous study has revealed that miR-155 serves an important role in the progression of clear-cell renal cell carcinoma (ccRCC); however, the underlying mechanism was not completely clarified. The prese...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443202/ https://www.ncbi.nlm.nih.gov/pubmed/28565840 http://dx.doi.org/10.3892/etm.2017.4263 |
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author | Ji, Hong Tian, Dong Zhang, Bing Zhang, Yangyang Yan, Dongliang Wu, Shuhua |
author_facet | Ji, Hong Tian, Dong Zhang, Bing Zhang, Yangyang Yan, Dongliang Wu, Shuhua |
author_sort | Ji, Hong |
collection | PubMed |
description | MicroRNA-155 (miR-155) is overexpressed in numerous human cancer types and has an oncogenic role. Previous study has revealed that miR-155 serves an important role in the progression of clear-cell renal cell carcinoma (ccRCC); however, the underlying mechanism was not completely clarified. The present study aimed to investigate the biological role of miR-155 in ccRCC and the underlying molecular mechanisms. The expression of miR-155 in 20 ccRCC and adjacent normal kidney tissues was determined by PCR. After downregulation of miR-155 expression by miR-155 inhibitor, cell growth was assessed by MTT and colony formation assays. Apoptosis and cell cycle distribution were analyzed by flow cytometry. Cell invasion and migration was detected by wound healing and Transwell assays. Furthermore, forkhead box O3a (FOXO3a) mRNA and protein expression were detected by PCR and immunoblotting. The expression of FOXO3a in 20 ccRCC tissues was also examined by immunohistochemistry. The expression of miR-155 was upregulated in ccRCC tissues compared to that in adjacent normal tissues. Inhibition of miR-155 significantly suppressed the proliferation, colony formation, migration and invasion, and induced G1 arrest and apoptosis of ccRCC cells in vitro. Moreover, inhibition of miR-155 significantly upregulated FOXO3a expression, and miR-155 expression was inversely correlated with FOXO3a expression in ccRCC tissues. In conclusion, miR-155 may have an important role in the genesis of ccRCC through targeting FOXO3a and may be a potential target for ccRCC therapy. |
format | Online Article Text |
id | pubmed-5443202 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54432022017-05-30 Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a Ji, Hong Tian, Dong Zhang, Bing Zhang, Yangyang Yan, Dongliang Wu, Shuhua Exp Ther Med Articles MicroRNA-155 (miR-155) is overexpressed in numerous human cancer types and has an oncogenic role. Previous study has revealed that miR-155 serves an important role in the progression of clear-cell renal cell carcinoma (ccRCC); however, the underlying mechanism was not completely clarified. The present study aimed to investigate the biological role of miR-155 in ccRCC and the underlying molecular mechanisms. The expression of miR-155 in 20 ccRCC and adjacent normal kidney tissues was determined by PCR. After downregulation of miR-155 expression by miR-155 inhibitor, cell growth was assessed by MTT and colony formation assays. Apoptosis and cell cycle distribution were analyzed by flow cytometry. Cell invasion and migration was detected by wound healing and Transwell assays. Furthermore, forkhead box O3a (FOXO3a) mRNA and protein expression were detected by PCR and immunoblotting. The expression of FOXO3a in 20 ccRCC tissues was also examined by immunohistochemistry. The expression of miR-155 was upregulated in ccRCC tissues compared to that in adjacent normal tissues. Inhibition of miR-155 significantly suppressed the proliferation, colony formation, migration and invasion, and induced G1 arrest and apoptosis of ccRCC cells in vitro. Moreover, inhibition of miR-155 significantly upregulated FOXO3a expression, and miR-155 expression was inversely correlated with FOXO3a expression in ccRCC tissues. In conclusion, miR-155 may have an important role in the genesis of ccRCC through targeting FOXO3a and may be a potential target for ccRCC therapy. D.A. Spandidos 2017-05 2017-03-24 /pmc/articles/PMC5443202/ /pubmed/28565840 http://dx.doi.org/10.3892/etm.2017.4263 Text en Copyright: © Ji 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 Ji, Hong Tian, Dong Zhang, Bing Zhang, Yangyang Yan, Dongliang Wu, Shuhua Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title | Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title_full | Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title_fullStr | Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title_full_unstemmed | Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title_short | Overexpression of miR-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting FOXO3a |
title_sort | overexpression of mir-155 in clear-cell renal cell carcinoma and its oncogenic effect through targeting foxo3a |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443202/ https://www.ncbi.nlm.nih.gov/pubmed/28565840 http://dx.doi.org/10.3892/etm.2017.4263 |
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