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Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin
Endometrial cancer is a life-threatening malignancy that affects women all over the world, and it has an increasing incidence. MicroRNAs (miRNAs/miRs) have been reported to be involved in cellular activities in endometrial cancer. The present study aimed to examine the effects of miR-183-5p on the e...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192766/ https://www.ncbi.nlm.nih.gov/pubmed/30226564 http://dx.doi.org/10.3892/ijmm.2018.3853 |
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author | Yan, Hua Sun, Bing-Mei Zhang, Yu-Ying Li, Yu-Juan Huang, Cheng-Xiang Feng, Fu-Zhong Li, Cui |
author_facet | Yan, Hua Sun, Bing-Mei Zhang, Yu-Ying Li, Yu-Juan Huang, Cheng-Xiang Feng, Fu-Zhong Li, Cui |
author_sort | Yan, Hua |
collection | PubMed |
description | Endometrial cancer is a life-threatening malignancy that affects women all over the world, and it has an increasing incidence. MicroRNAs (miRNAs/miRs) have been reported to be involved in cellular activities in endometrial cancer. The present study aimed to examine the effects of miR-183-5p on the epithelial-mesenchymal transition (EMT), proliferation, invasion, migration and apoptosis of human endometrial cancer cells by targeting Ezrin. Primary endometrial cancer tissues and adjacent normal tissues were obtained for the investigation. The protein expression of Ezrin in tissues was detected by immunohistochemistry. The expression level of miR-183-5p and the mRNA and protein expression levels of Ezrin and EMT-associated genes were determined by reverse transcription-quantitative polymerase chain reaction and western blot analyses. Endometrial cancer cells were treated with miR-183-5p inhibitors, small interfering RNA targeting Ezrin or miR-183-5p inhibitors. Cell proliferation, cell cycle, apoptosis, migration and invasion were then evaluated using an MTT assay, flow cytometry, scratch test and Transwell assay, respectively. Compared with normal adjacent tissues, the expression of miR-183-5p was decreased in endometrial cancer tissues, and the expression of Ezrin was significantly increased in endometrial cancer tissues. The protein expression of Ezrin was correlated with the severity and poor prognosis of endometrial cancer. Notably, the target prediction program and the luciferase reporter gene assay confirmed that miR-183-5p targeted and negatively regulated the expression of Ezrin. In vivo experiments revealed that the increased expression of miR-183-5p and decreased expression of Ezrin inhibited EMT, cell proliferation, migration and invasion, but promoted cell apoptosis in Ishikawa cells. These results suggested that the upregulated expression of miR-183-5p promoted apoptosis and suppressed the EMT, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin. |
format | Online Article Text |
id | pubmed-6192766 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61927662018-10-22 Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Yan, Hua Sun, Bing-Mei Zhang, Yu-Ying Li, Yu-Juan Huang, Cheng-Xiang Feng, Fu-Zhong Li, Cui Int J Mol Med Articles Endometrial cancer is a life-threatening malignancy that affects women all over the world, and it has an increasing incidence. MicroRNAs (miRNAs/miRs) have been reported to be involved in cellular activities in endometrial cancer. The present study aimed to examine the effects of miR-183-5p on the epithelial-mesenchymal transition (EMT), proliferation, invasion, migration and apoptosis of human endometrial cancer cells by targeting Ezrin. Primary endometrial cancer tissues and adjacent normal tissues were obtained for the investigation. The protein expression of Ezrin in tissues was detected by immunohistochemistry. The expression level of miR-183-5p and the mRNA and protein expression levels of Ezrin and EMT-associated genes were determined by reverse transcription-quantitative polymerase chain reaction and western blot analyses. Endometrial cancer cells were treated with miR-183-5p inhibitors, small interfering RNA targeting Ezrin or miR-183-5p inhibitors. Cell proliferation, cell cycle, apoptosis, migration and invasion were then evaluated using an MTT assay, flow cytometry, scratch test and Transwell assay, respectively. Compared with normal adjacent tissues, the expression of miR-183-5p was decreased in endometrial cancer tissues, and the expression of Ezrin was significantly increased in endometrial cancer tissues. The protein expression of Ezrin was correlated with the severity and poor prognosis of endometrial cancer. Notably, the target prediction program and the luciferase reporter gene assay confirmed that miR-183-5p targeted and negatively regulated the expression of Ezrin. In vivo experiments revealed that the increased expression of miR-183-5p and decreased expression of Ezrin inhibited EMT, cell proliferation, migration and invasion, but promoted cell apoptosis in Ishikawa cells. These results suggested that the upregulated expression of miR-183-5p promoted apoptosis and suppressed the EMT, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin. D.A. Spandidos 2018-11 2018-09-04 /pmc/articles/PMC6192766/ /pubmed/30226564 http://dx.doi.org/10.3892/ijmm.2018.3853 Text en Copyright: © Yan 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 Yan, Hua Sun, Bing-Mei Zhang, Yu-Ying Li, Yu-Juan Huang, Cheng-Xiang Feng, Fu-Zhong Li, Cui Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title | Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title_full | Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title_fullStr | Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title_full_unstemmed | Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title_short | Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin |
title_sort | upregulation of mir-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating ezrin |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192766/ https://www.ncbi.nlm.nih.gov/pubmed/30226564 http://dx.doi.org/10.3892/ijmm.2018.3853 |
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