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Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells
Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in He...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4962058/ https://www.ncbi.nlm.nih.gov/pubmed/27460655 http://dx.doi.org/10.1038/srep30496 |
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author | Li, Xv Wang, Yajun Xiong, Yuzhen Wu, Jun Ding, Hang Chen, Xiaoyi Lan, Liubo Zhang, Haitao |
author_facet | Li, Xv Wang, Yajun Xiong, Yuzhen Wu, Jun Ding, Hang Chen, Xiaoyi Lan, Liubo Zhang, Haitao |
author_sort | Li, Xv |
collection | PubMed |
description | Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in HepG2 cells. But this autophagy was inhibited by inactivation of SIRT1 meanwhile, galangin failed to reduce the acetylation of endogenous LC3 after SIRT1 was knocked-down. Collectively, these findings demonstrate a new mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1. |
format | Online Article Text |
id | pubmed-4962058 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49620582016-08-08 Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells Li, Xv Wang, Yajun Xiong, Yuzhen Wu, Jun Ding, Hang Chen, Xiaoyi Lan, Liubo Zhang, Haitao Sci Rep Article Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in HepG2 cells. But this autophagy was inhibited by inactivation of SIRT1 meanwhile, galangin failed to reduce the acetylation of endogenous LC3 after SIRT1 was knocked-down. Collectively, these findings demonstrate a new mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1. Nature Publishing Group 2016-07-27 /pmc/articles/PMC4962058/ /pubmed/27460655 http://dx.doi.org/10.1038/srep30496 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Li, Xv Wang, Yajun Xiong, Yuzhen Wu, Jun Ding, Hang Chen, Xiaoyi Lan, Liubo Zhang, Haitao Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title | Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title_full | Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title_fullStr | Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title_full_unstemmed | Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title_short | Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells |
title_sort | galangin induces autophagy via deacetylation of lc3 by sirt1 in hepg2 cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4962058/ https://www.ncbi.nlm.nih.gov/pubmed/27460655 http://dx.doi.org/10.1038/srep30496 |
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