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miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells
The present study investigated the effect of microRNA (miR)-15a-3p on the proliferation, migration and apoptosis of lens epithelial cells and its potential mechanism, in order to further elucidate the pathogenesis of age-related cataracts (ARCs). The HLE-B3 human lens epithelial cell line was transf...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323217/ https://www.ncbi.nlm.nih.gov/pubmed/30569090 http://dx.doi.org/10.3892/mmr.2018.9738 |
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author | Liu, Shu-Jun Wang, Wen-Ting Zhang, Feng-Lan Yu, Yong-Hong Yu, Hua-Jun Liang, Yan Li, Ning Li, Yuan-Bin |
author_facet | Liu, Shu-Jun Wang, Wen-Ting Zhang, Feng-Lan Yu, Yong-Hong Yu, Hua-Jun Liang, Yan Li, Ning Li, Yuan-Bin |
author_sort | Liu, Shu-Jun |
collection | PubMed |
description | The present study investigated the effect of microRNA (miR)-15a-3p on the proliferation, migration and apoptosis of lens epithelial cells and its potential mechanism, in order to further elucidate the pathogenesis of age-related cataracts (ARCs). The HLE-B3 human lens epithelial cell line was transfected with miR-15a-3p mimic. Expression of the miR-15a-3p mimic was measured by fluorescence-based reverse transcription-quantitative polymerase chain reaction analysis. Cell proliferation, apoptosis, invasion and migration were investigated using MTT and plate clone formation assays, terminal deoxynucleotidyl transferase dUTP nick end labeling and flow cytometry, and a wound healing assay and Transwell assay, respectively. The protein expression levels of B-cell lymphoma 2 (BCL2) and myeloid cell leukemia sequence 1 (MCL1) were also compared between transfected and wild-type HLE-B3 cells by western blot analysis. The results showed that transfection with the miR-15a-3p mimic significantly suppressed the proliferation of HLE-B3 cells, induced cell apoptosis and increased the proportion of early apoptotic cells. The migration of HLE-B3 cells was significantly inhibited following transfection with miR-15a-3p mimic (P<0.01), whereas cell invasion was unaffected (P>0.05). In addition, reduced protein levels of BCL2 and MCL1 were observed in the miR-15a-3p mimic-transfected HLE-B3 cells (P<0.01). In conclusion, miR-15a-3p may suppress cell proliferation and migration, and induce cell apoptosis in lens epithelial cells through inhibiting the expression of BCL2 and MCL1, which contributes to the onset of ARCs. |
format | Online Article Text |
id | pubmed-6323217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63232172019-01-15 miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells Liu, Shu-Jun Wang, Wen-Ting Zhang, Feng-Lan Yu, Yong-Hong Yu, Hua-Jun Liang, Yan Li, Ning Li, Yuan-Bin Mol Med Rep Articles The present study investigated the effect of microRNA (miR)-15a-3p on the proliferation, migration and apoptosis of lens epithelial cells and its potential mechanism, in order to further elucidate the pathogenesis of age-related cataracts (ARCs). The HLE-B3 human lens epithelial cell line was transfected with miR-15a-3p mimic. Expression of the miR-15a-3p mimic was measured by fluorescence-based reverse transcription-quantitative polymerase chain reaction analysis. Cell proliferation, apoptosis, invasion and migration were investigated using MTT and plate clone formation assays, terminal deoxynucleotidyl transferase dUTP nick end labeling and flow cytometry, and a wound healing assay and Transwell assay, respectively. The protein expression levels of B-cell lymphoma 2 (BCL2) and myeloid cell leukemia sequence 1 (MCL1) were also compared between transfected and wild-type HLE-B3 cells by western blot analysis. The results showed that transfection with the miR-15a-3p mimic significantly suppressed the proliferation of HLE-B3 cells, induced cell apoptosis and increased the proportion of early apoptotic cells. The migration of HLE-B3 cells was significantly inhibited following transfection with miR-15a-3p mimic (P<0.01), whereas cell invasion was unaffected (P>0.05). In addition, reduced protein levels of BCL2 and MCL1 were observed in the miR-15a-3p mimic-transfected HLE-B3 cells (P<0.01). In conclusion, miR-15a-3p may suppress cell proliferation and migration, and induce cell apoptosis in lens epithelial cells through inhibiting the expression of BCL2 and MCL1, which contributes to the onset of ARCs. D.A. Spandidos 2019-02 2018-12-11 /pmc/articles/PMC6323217/ /pubmed/30569090 http://dx.doi.org/10.3892/mmr.2018.9738 Text en Copyright: © Liu 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 Liu, Shu-Jun Wang, Wen-Ting Zhang, Feng-Lan Yu, Yong-Hong Yu, Hua-Jun Liang, Yan Li, Ning Li, Yuan-Bin miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title | miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title_full | miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title_fullStr | miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title_full_unstemmed | miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title_short | miR-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
title_sort | mir-15a-3p affects the proliferation, migration and apoptosis of lens epithelial cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323217/ https://www.ncbi.nlm.nih.gov/pubmed/30569090 http://dx.doi.org/10.3892/mmr.2018.9738 |
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