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miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells
OBJECTIVE: To investigate the role of miR-21 in cyclooxygenase-2 inhibitor NS398-induced apoptosis and invasion in gastric cancer (GC) cells. METHODS: AGS cells were treated with NS398 and transfected with miR-21. Quantitative real-time polymerase chain reaction was used to measure miR-21 mRNA expre...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640150/ https://www.ncbi.nlm.nih.gov/pubmed/26604791 http://dx.doi.org/10.2147/OTT.S90012 |
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author | Li, Huanqing Cheng, Jian Mao, Yuqing Jiang, Miao Fan, Xiaoming |
author_facet | Li, Huanqing Cheng, Jian Mao, Yuqing Jiang, Miao Fan, Xiaoming |
author_sort | Li, Huanqing |
collection | PubMed |
description | OBJECTIVE: To investigate the role of miR-21 in cyclooxygenase-2 inhibitor NS398-induced apoptosis and invasion in gastric cancer (GC) cells. METHODS: AGS cells were treated with NS398 and transfected with miR-21. Quantitative real-time polymerase chain reaction was used to measure miR-21 mRNA expression. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling and flow cytometric analysis. The protein expression of cleaved caspase-3, Bcl-2, Bax, Bak, and PTEN was detected by Western blot. The capacities for invasion and migration were measured by transwell and wound-healing assays, respectively. RESULTS: Treatment of AGS cells with NS398 induced apoptosis in a dose-dependent manner accompanied by significant downregulation of miR-21 mRNA expression. Upregulation of miR-21 expression by transfection of miR-21 mimics into AGS cells blocked NS398-induced apoptosis. Treatment of AGS cells with NS398 induced changes in Bcl-2 protein family members, showing an increase in the protein expression of Bax, Bak, and PTEN, with a concomitant decrease in the protein expression of Bcl-2. In cells transfected with miR-21 mimics, these changes were reversed. The decrease in cellular invasiveness and migration induced by NS398 was blocked by upregulation of miR-21. CONCLUSION: miR-21 mediates anticancer effects of NS398 in GC cells by regulating apoptosis-related proteins. miR-21 is one of the molecular targets of this specific cyclooxygenase-2 inhibitor in the prevention and treatment of GC. |
format | Online Article Text |
id | pubmed-4640150 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-46401502015-11-24 miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells Li, Huanqing Cheng, Jian Mao, Yuqing Jiang, Miao Fan, Xiaoming Onco Targets Ther Original Research OBJECTIVE: To investigate the role of miR-21 in cyclooxygenase-2 inhibitor NS398-induced apoptosis and invasion in gastric cancer (GC) cells. METHODS: AGS cells were treated with NS398 and transfected with miR-21. Quantitative real-time polymerase chain reaction was used to measure miR-21 mRNA expression. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling and flow cytometric analysis. The protein expression of cleaved caspase-3, Bcl-2, Bax, Bak, and PTEN was detected by Western blot. The capacities for invasion and migration were measured by transwell and wound-healing assays, respectively. RESULTS: Treatment of AGS cells with NS398 induced apoptosis in a dose-dependent manner accompanied by significant downregulation of miR-21 mRNA expression. Upregulation of miR-21 expression by transfection of miR-21 mimics into AGS cells blocked NS398-induced apoptosis. Treatment of AGS cells with NS398 induced changes in Bcl-2 protein family members, showing an increase in the protein expression of Bax, Bak, and PTEN, with a concomitant decrease in the protein expression of Bcl-2. In cells transfected with miR-21 mimics, these changes were reversed. The decrease in cellular invasiveness and migration induced by NS398 was blocked by upregulation of miR-21. CONCLUSION: miR-21 mediates anticancer effects of NS398 in GC cells by regulating apoptosis-related proteins. miR-21 is one of the molecular targets of this specific cyclooxygenase-2 inhibitor in the prevention and treatment of GC. Dove Medical Press 2015-11-04 /pmc/articles/PMC4640150/ /pubmed/26604791 http://dx.doi.org/10.2147/OTT.S90012 Text en © 2015 Li et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Li, Huanqing Cheng, Jian Mao, Yuqing Jiang, Miao Fan, Xiaoming miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title | miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title_full | miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title_fullStr | miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title_full_unstemmed | miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title_short | miR-21 inhibits the effects of cyclooxygenase-2 inhibitor NS398 on apoptosis and invasion in gastric cancer cells |
title_sort | mir-21 inhibits the effects of cyclooxygenase-2 inhibitor ns398 on apoptosis and invasion in gastric cancer cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640150/ https://www.ncbi.nlm.nih.gov/pubmed/26604791 http://dx.doi.org/10.2147/OTT.S90012 |
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