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Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway
Caffeine is one of the most widely consumed substances found in beverages, and has demonstrated anticancer effects in several types of cancer. The present study aimed to examine the anticancer effects of caffeine on gastric cancer (GC) cells (MGC-803 and SGC-7901) in vitro, and to determine whether...
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/PMC5547974/ https://www.ncbi.nlm.nih.gov/pubmed/28677810 http://dx.doi.org/10.3892/mmr.2017.6894 |
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author | Liu, Hanyang Zhou, Yan Tang, Liming |
author_facet | Liu, Hanyang Zhou, Yan Tang, Liming |
author_sort | Liu, Hanyang |
collection | PubMed |
description | Caffeine is one of the most widely consumed substances found in beverages, and has demonstrated anticancer effects in several types of cancer. The present study aimed to examine the anticancer effects of caffeine on gastric cancer (GC) cells (MGC-803 and SGC-7901) in vitro, and to determine whether the apoptosis-related caspase-9/−3 pathway is associated with these effects. The sustained antiproliferative effects of caffeine on gastric cancer were also investigated. GC cell viability and proliferation were evaluated using cell counting and colony forming assays, following treatment with various concentrations of caffeine. Flow cytometry was performed to assess cell cycle dynamics and apoptosis. Western blot analysis was conducted to detect the activity of the caspase-9/−3 pathway. The results indicated that caffeine treatment significantly suppressed GC cell growth and viability and induced apoptosis by activating the caspase-9/−3 pathway. Furthermore, the anticancer effects of caffeine appeared to be sustained, as the caspase-9/−3 pathway remained active following caffeine withdrawal. In conclusion, caffeine may function as a sustained anticancer agent by activating the caspase-9/−3 pathway, which indicates that it may be useful as a therapeutic candidate in gastric cancer. |
format | Online Article Text |
id | pubmed-5547974 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-55479742017-10-24 Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway Liu, Hanyang Zhou, Yan Tang, Liming Mol Med Rep Articles Caffeine is one of the most widely consumed substances found in beverages, and has demonstrated anticancer effects in several types of cancer. The present study aimed to examine the anticancer effects of caffeine on gastric cancer (GC) cells (MGC-803 and SGC-7901) in vitro, and to determine whether the apoptosis-related caspase-9/−3 pathway is associated with these effects. The sustained antiproliferative effects of caffeine on gastric cancer were also investigated. GC cell viability and proliferation were evaluated using cell counting and colony forming assays, following treatment with various concentrations of caffeine. Flow cytometry was performed to assess cell cycle dynamics and apoptosis. Western blot analysis was conducted to detect the activity of the caspase-9/−3 pathway. The results indicated that caffeine treatment significantly suppressed GC cell growth and viability and induced apoptosis by activating the caspase-9/−3 pathway. Furthermore, the anticancer effects of caffeine appeared to be sustained, as the caspase-9/−3 pathway remained active following caffeine withdrawal. In conclusion, caffeine may function as a sustained anticancer agent by activating the caspase-9/−3 pathway, which indicates that it may be useful as a therapeutic candidate in gastric cancer. D.A. Spandidos 2017-09 2017-06-30 /pmc/articles/PMC5547974/ /pubmed/28677810 http://dx.doi.org/10.3892/mmr.2017.6894 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, Hanyang Zhou, Yan Tang, Liming Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title | Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title_full | Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title_fullStr | Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title_full_unstemmed | Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title_short | Caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
title_sort | caffeine induces sustained apoptosis of human gastric cancer cells by activating the caspase-9/caspase-3 signalling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547974/ https://www.ncbi.nlm.nih.gov/pubmed/28677810 http://dx.doi.org/10.3892/mmr.2017.6894 |
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