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Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells
Regular use of aspirin can reduce cancer incidence, recurrence, metastasis and cancer-related mortality. Aspirin suppresses proliferation and induces apoptosis and autophagy in colorectal cancer cells, but the precise mechanism is not clear. In this study, we demonstrated that aspirin induced autoph...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650378/ https://www.ncbi.nlm.nih.gov/pubmed/29088823 http://dx.doi.org/10.18632/oncotarget.20367 |
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author | Sun, Ting Ming, Liang Yan, Yunmeng Zhang, Yan Xue, Haikuo |
author_facet | Sun, Ting Ming, Liang Yan, Yunmeng Zhang, Yan Xue, Haikuo |
author_sort | Sun, Ting |
collection | PubMed |
description | Regular use of aspirin can reduce cancer incidence, recurrence, metastasis and cancer-related mortality. Aspirin suppresses proliferation and induces apoptosis and autophagy in colorectal cancer cells, but the precise mechanism is not clear. In this study, we demonstrated that aspirin induced autophagosome formation in colorectal cancer cells, but autophagic degradation was blocked through aspirin-mediated Beclin 1 acetylation. Blocked autophagic degradation weakened aspirin-induced cell death. Collectively, our findings indicate the dual roles of aspirin on autophagy, and demonstrate a new mechanism by which Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells. |
format | Online Article Text |
id | pubmed-5650378 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-56503782017-10-30 Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells Sun, Ting Ming, Liang Yan, Yunmeng Zhang, Yan Xue, Haikuo Oncotarget Research Paper Regular use of aspirin can reduce cancer incidence, recurrence, metastasis and cancer-related mortality. Aspirin suppresses proliferation and induces apoptosis and autophagy in colorectal cancer cells, but the precise mechanism is not clear. In this study, we demonstrated that aspirin induced autophagosome formation in colorectal cancer cells, but autophagic degradation was blocked through aspirin-mediated Beclin 1 acetylation. Blocked autophagic degradation weakened aspirin-induced cell death. Collectively, our findings indicate the dual roles of aspirin on autophagy, and demonstrate a new mechanism by which Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells. Impact Journals LLC 2017-08-19 /pmc/articles/PMC5650378/ /pubmed/29088823 http://dx.doi.org/10.18632/oncotarget.20367 Text en Copyright: © 2017 Sun et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Sun, Ting Ming, Liang Yan, Yunmeng Zhang, Yan Xue, Haikuo Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title | Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title_full | Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title_fullStr | Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title_full_unstemmed | Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title_short | Beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
title_sort | beclin 1 acetylation impairs the anticancer effect of aspirin in colorectal cancer cells |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650378/ https://www.ncbi.nlm.nih.gov/pubmed/29088823 http://dx.doi.org/10.18632/oncotarget.20367 |
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